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          <?xml version='1.0' encoding='UTF-8'?><response><query>"http://purl.org/au-research/grants/NHMRC/1013667"</query><zone name="newspaper"><records s="0" n="0" total="0" /></zone><zone name="people"><records s="0" n="0" total="0" /></zone><zone name="list"><records s="0" n="0" total="0" /></zone><zone name="article"><records s="0" n="20" total="22" next="/result?q=%22http%3A%2F%2Fpurl.org%2Fau-research%2Fgrants%2FNHMRC%2F1013667%22&include=workversions&zone=article&s=20"><work id="183816326" url="/work/183816326"><troveUrl>http://trove.nla.gov.au/work/183816326</troveUrl><title>BRAF-targeted therapy and immune responses to melanoma</title><contributor>Ngiow, Shin Foong</contributor><contributor> Knight, Deborah A</contributor><contributor> Ribas, Antoni</contributor><contributor> McArthur, Grant A</contributor><contributor> Smyth, Mark J</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>1</versionCount><relevance score="0.01478266">limited relevance</relevance><version id="200210992 209155727"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/41497</identifier><datestamp>2017-08-28T14:26:39Z</datestamp><setSpec>com_11343_273</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_274</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>BRAF-targeted therapy and immune responses to melanoma</title>
<creator>Ngiow, SF</creator>
<creator>Knight, DA</creator>
<creator>Ribas, A</creator>
<creator>McArthur, GA</creator>
<creator>Smyth, MJ</creator>





<description>Fulltext embargoed for: 6 months post date of publication</description>
<dateAccepted>2014-08-19T01:29:09Z</dateAccepted>
<available>2014-08-19T01:29:09Z</available>
<created>2014-08-19T01:29:09Z</created>
<issued>2013-06-01</issued>
<type>journal article</type>
<publisher>LANDES BIOSCIENCE</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1002655</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>


<relation>
                    http://doi.org/10.4161/onci.24462</relation>
<isPartOf type="series">ONCOIMMUNOLOGY</isPartOf>
<bibliographicCitation type="volume">2</bibliographicCitation>
<bibliographicCitation type="issue">6</bibliographicCitation>
<bibliographicCitation type="issn">2162-4011</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013-06-01</bibliographicCitation>
<bibliographicCitation type="dateIssued">Jun-01</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/41497</identifier>
<subject>BRAF</subject><subject>checkpoint</subject><subject>immunity</subject><subject>melanoma</subject><subject>T cell</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><record><header>
      <identifier>oai:espace.library.uq.edu.au:UQ:306881</identifier>
      <datestamp>2017-11-03T08:11:23Z</datestamp>
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			    </header><metadata>
	      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	            <title>BRAF-targeted therapy and immune responses to melanoma</title>
	
		





	





	
	
	
        <bibliographicCitation>
        Ngiow, Shin Foong, Knight, Deborah A., Ribas, Antoni, McArthur, Grant A. and Smyth, Mark J. (2013) BRAF-targeted therapy and immune responses to melanoma. Oncoimmunology, 2 6: e24462.1-e24462.3. doi:10.4161/onci.24462
    </bibliographicCitation><relation>http://doi.org/10.4161/onci.24462
    </relation>
    
	
	
	

			<description>
					Type I BRAF inhibitors and immunotherapy constitute two new exciting approaches for the treatment of advanced malignant melanoma. We have recently elucidated a role for host C-C chemokine receptor Type 2 (CCR2) in the antineoplastic effects of Type I BRAF inhibitors in mice, supporting the therapeutic potential of combining BRAF inhibitors with immunotherapy.
				</description>
	
        <type>journal article</type>
        <date>2013-06-01</date>
																        <creator>Ngiow, Shin Foong</creator>
							        <creator>Knight, Deborah A.</creator>
							        <creator>Ribas, Antoni</creator>
							        <creator>McArthur, Grant A.</creator>
							        <creator>Smyth, Mark J.</creator>
											
																        <subject>BRAF</subject>
							        <subject>Checkpoint</subject>
							        <subject>Immunity</subject>
							        <subject>Melanoma</subject>
							        <subject>T cell</subject>
									        
		

		
		

						        	<publisher>Landes Bioscience</publisher>
												        			      			      <language>eng</language>
			      					

		


										            							        <identifier linktype="notonline">http://espace.library.uq.edu.au/view/UQ:306881</identifier>

		
	      </dc>
	




    </metadata><metadataSource type="nuc">QU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013-06-01</issued><holdingsCount>2</holdingsCount></version></work><work id="191549480" url="/work/191549480"><troveUrl>http://trove.nla.gov.au/work/191549480</troveUrl><title>CD1d-lipid antigen recognition by the γδ TCR</title><contributor>Uldrich, Adam P</contributor><contributor> Le Nours, Jérôme</contributor><contributor> Pellicci, Daniel G</contributor><contributor> Gherardin, Nicholas A</contributor><contributor> McPherson, Kirsty G</contributor><contributor> Lim, Ricky T</contributor><contributor> Patel, Onisha</contributor><contributor> BEDDOE, TRAVIS</contributor><contributor> Gras, Stephanie</contributor><contributor> ROSSJOHN, JAMIE</contributor><contributor> GODFREY, DALE I</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.012318883">limited relevance</relevance><snippet> in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><version id="209154785"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/39687</identifier>
                <datestamp>2017-02-16T20:54:22Z</datestamp>
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<title>CD1d-lipid antigen recognition by the γδ TCR</title>
<creator>Uldrich, Adam P.</creator>
<creator>Le Nours, Jérôme</creator>
<creator>Pellicci, Daniel G.</creator>
<creator>Gherardin, Nicholas A.</creator>
<creator>McPherson, Kirsty G.</creator>
<creator>Lim, Ricky T.</creator>
<creator>Patel, Onisha</creator>
<creator>BEDDOE, TRAVIS</creator>
<creator>Gras, Stephanie</creator>
<creator>ROSSJOHN, JAMIE</creator>
<creator>GODFREY, DALE I.</creator>










<abstract>The T cell repertoire comprises αβ and γδ T cell lineages. Although it is established how αβ T cell antigen receptors (TCRs) interact with antigen presented by antigen-presenting molecules, this is unknown for γδ TCRs. We describe a population of human Vδ1+ γδ T cells that exhibit autoreactivity to CD1d and provide a molecular basis for how a γδ TCR binds CD1d–α-galactosylceramide (α-GalCer). The γδ TCR docked orthogonally, over the A′ pocket of CD1d, in which the Vδ1-chain, and in particular the germ line–encoded CDR1δ loop, dominated interactions with CD1d. The TCR γ-chain sat peripherally to the interface, with the CDR3γ loop representing the principal determinant for α-GalCer specificity. Accordingly, we provide insight into how a γδ TCR binds specifically to a lipid-loaded antigen-presenting molecule.</abstract>
<description>Published Version</description>
<description>© 2013 Nature America, Inc. All rights reserved.</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:53:19Z</dateAccepted>
<available>2014-06-16T15:53:19Z</available>
<created>2014-06-16T15:53:19Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Nature Publishing Group</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
					http://doi.org/10.1038/ni.2713</relation>
<isPartOf type="series">Nature Immunology</isPartOf>
<bibliographicCitation type="volume">14</bibliographicCitation>
<bibliographicCitation type="issue">11</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39687</identifier>
<subject>T-cell-receptor</subject><subject>crystal-structure</subject><subject>NKT cells</subject><subject>structural basis</subject><subject>CD1d</subject><subject>T22</subject><subject>lymphocytes</subject><subject>reactivity</subject><subject>complexes</subject><subject>selection</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="204614465" url="/work/204614465"><troveUrl>http://trove.nla.gov.au/work/204614465</troveUrl><title>Identification of a Potent Microbial Lipid Antigen for Diverse NKT Cells</title><contributor>Wolf, Benjamin</contributor><contributor> Tatituri, Raju</contributor><contributor> Almeida, Catarina</contributor><contributor> Le Nours, Jerome</contributor><contributor> Bhowruth, Veemal</contributor><contributor> Johnson, Darryl</contributor><contributor> Uldrich, Adam</contributor><contributor> Hsu, Fong-Fu</contributor><contributor> Brigl, Manfred</contributor><contributor> Besra, Gurdyal</contributor><contributor> Rossjohn, Jamie</contributor><contributor> Godfrey, Dale</contributor><contributor> Brenner, Michael</contributor><issued>2015</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.012318883">limited relevance</relevance><identifier type="url" linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/1243820</identifier><version id="224609383"><record><header>
        <identifier>monash:166151</identifier>
        <datestamp>2016-02-25T23:29:41.026Z</datestamp>
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      </header><metadata>
      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>Identification of a Potent Microbial Lipid Antigen for Diverse NKT Cells</title><creator>Wolf, Benjamin</creator><creator>Tatituri, Raju</creator><creator>Almeida, Catarina</creator><creator>Le Nours, Jerome</creator><creator>Bhowruth, Veemal</creator><creator>Johnson, Darryl</creator><creator>Uldrich, Adam</creator><creator>Hsu, Fong-Fu</creator><creator>Brigl, Manfred</creator><creator>Besra, Gurdyal</creator><creator>Rossjohn, Jamie</creator><creator>Godfrey, Dale</creator><creator>Brenner, Michael</creator><subject>Immunology (1107)</subject><publisher>American Association of Immunologists</publisher><date>2015</date><type>text</type><type>journal article</type><identifier linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/1243820</identifier><identifier>monash:166151</identifier><language>eng</language><relation>Journal Of Immunology [P], vol. 195, no. 6, p. 2540-2551</relation><relation>urn:ISSN:0022-1767</relation></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2015</issued><holdingsCount>1</holdingsCount></version><version id="248945604"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/168275</identifier>
                <datestamp>2017-06-26T05:20:58Z</datestamp>
                <setSpec>com_11343_225</setSpec>
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                <setSpec>com_11343_163</setSpec>
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            </header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>Identification of a Potent Microbial Lipid Antigen for Diverse NKT Cells</title>
<creator>GODFREY, DALE</creator>
<creator>ULDRICH, ADAM</creator>
<abstract>Semi-invariant/type I NKT cells are a well-characterized CD1d-restricted T cell subset. The availability of potent Ags and tetramers for semi-invariant/type I NKT cells allowed this population to be extensively studied and revealed their central roles in infection, autoimmunity, and tumor immunity. In contrast, diverse/type II NKT (dNKT) cells are poorly understood because the lipid Ags that they recognize are largely unknown. We sought to identify dNKT cell lipid Ag(s) by interrogating a panel of dNKT mouse cell hybridomas with lipid extracts from the pathogen Listeria monocytogenes. We identified Listeria phosphatidylglycerol as a microbial Ag that was significantly more potent than a previously characterized dNKT cell Ag, mammalian phosphatidylglycerol. Further, although mammalian phosphatidylglycerol-loaded CD1d tetramers did not stain dNKT cells, the Listeria-derived phosphatidylglycerol-loaded tetramers did. The structure of Listeria phosphatidylglycerol was distinct from mammalian phosphatidylglycerol because it contained shorter, fully-saturated anteiso fatty acid lipid tails. CD1d-binding lipid-displacement studies revealed that the microbial phosphatidylglycerol Ag binds significantly better to CD1d than do counterparts with the same headgroup. These data reveal a highly potent microbial lipid Ag for a subset of dNKT cells and provide an explanation for its increased Ag potency compared with the mammalian counterpart.</abstract>
<dateAccepted>2017-06-16T01:46:39Z</dateAccepted>
<available>2017-06-16T01:46:39Z</available>
<created>2017-06-16T01:46:39Z</created>
<issued>2015-09-15</issued>
<type>journal article</type>
<publisher>AMER ASSOC IMMUNOLOGISTS</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1021972</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
					http://purl.org/au-research/grants/ARC/FT140100278</relation>
<relation>
					http://purl.org/au-research/grants/ARC/FT140100278</relation>
<relation>
					http://orcid.org/0000-0002-3009-5472</relation>
<relation>
					http://orcid.org/0000-0002-6350-5976</relation>
<relation>
					http://doi.org/10.4049/jimmunol.1501019</relation>
<isPartOf type="series">JOURNAL OF IMMUNOLOGY</isPartOf>
<bibliographicCitation type="volume">195</bibliographicCitation>
<bibliographicCitation type="issue">6</bibliographicCitation>
<bibliographicCitation type="issn">0022-1767</bibliographicCitation>
<bibliographicCitation type="yearIssued">2015-09-15</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/168275</identifier>
</qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2015-09-15</issued><holdingsCount>1</holdingsCount></version></work><work id="179334907" url="/work/179334907"><troveUrl>http://trove.nla.gov.au/work/179334907</troveUrl><title>Recognition of CD1d-restricted antigens by natural killer T cells</title><contributor>Rossjohn, J</contributor><contributor> Pellicci, DG</contributor><contributor> Patel, O</contributor><contributor> Gapin, L</contributor><contributor> Godfrey, DI</contributor><issued>2012</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.012318883">limited relevance</relevance><snippet> and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><identifier type="url" linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/822308</identifier><version id="195199245"><record><header>
        <identifier>monash:111742</identifier>
        <datestamp>2015-02-03T03:11:40.723Z</datestamp>
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      </header><metadata>
      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>Recognition of CD1d-restricted antigens by natural killer T cells</title><creator>Rossjohn, Jamie</creator><creator>Pellicci, Daniel</creator><creator>Patel, Onisha</creator><creator>Gapin, Laurent</creator><creator>Godfrey, Dale</creator><subject>Immunology (1107)</subject><publisher>Nature Publishing Group</publisher><date>2012</date><type>text</type><type>journal article</type><identifier linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/822308</identifier><identifier>monash:111742</identifier><language>eng</language><relation>Nature Reviews Immunology [P], vol. 12, no. 12, p. 845-857</relation><relation>urn:ISSN:14741733</relation><rights>Subscription access to fulltext</rights></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2012</issued><holdingsCount>1</holdingsCount></version><version id="209154783"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/39685</identifier><datestamp>2017-08-28T21:11:56Z</datestamp><setSpec>com_11343_225</setSpec><setSpec>com_11343_164</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_226</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>Recognition of CD1d-restricted antigens by natural killer T cells</title>
<creator>Rossjohn, J</creator>
<creator>Pellicci, DG</creator>
<creator>Patel, O</creator>
<creator>Gapin, L</creator>
<creator>Godfrey, DI</creator>










<abstract>Natural killer T (NKT) cells are innate-like T cells that rapidly produce a variety of cytokines following T cell receptor (TCR) activation and can shape the immune response in many different settings. There are two main NKT cell subsets: type I NKT cells are typically characterized by the expression of a semi-invariant TCR, whereas the TCRs expressed by type II NKT cells are more diverse. This Review focuses on the defining features and emerging generalities regarding how NKT cells specifically recognize self, microbial and synthetic lipid-based antigens that are presented by CD1d. Such information is vitally important to better understand, and fully harness, the therapeutic potential of NKT cells.</abstract>
<description>Published Version</description>
<description>© 2012 Macmillan Publishers Limited. All rights reserved</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:53:10Z</dateAccepted>
<available>2014-06-16T15:53:10Z</available>
<created>2014-06-16T15:53:10Z</created>
<issued>2012-12-01</issued>
<type>journal article</type>
<publisher>NATURE PUBLISHING GROUP</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1021972</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>

<relation>
                    http://orcid.org/0000-0002-3009-5472</relation>
<relation>
                    http://doi.org/10.1038/nri3328</relation>
<isPartOf type="series">NATURE REVIEWS IMMUNOLOGY</isPartOf>
<bibliographicCitation type="volume">12</bibliographicCitation>
<bibliographicCitation type="issue">12</bibliographicCitation>
<bibliographicCitation type="issn">1474-1733</bibliographicCitation>
<bibliographicCitation type="yearIssued">2012-12-01</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39685</identifier>
<subject>major histocompatibility complex</subject><subject>invariant NKT cells</subject><subject>mycobacterial phosphatidylinositol mannoside</subject><subject>alpha-galactosylceramide</subject><subject>crystal-structure</subject><subject>mouse CD1</subject><subject>receptor recognition</subject><subject>glycolipid antigens</subject><subject>structural insight</subject><subject>self glycolipids</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2012-12-01</issued><holdingsCount>1</holdingsCount></version></work><work id="202874436" url="/work/202874436"><troveUrl>http://trove.nla.gov.au/work/202874436</troveUrl><title>DNAM-1 Expression Marks an Alternative Program of NK Cell Maturation</title><contributor>Martinet, Ludovic</contributor><contributor> FerrariDeAndrade, Lucas</contributor><contributor> Guillerey, Camille</contributor><contributor> Lee, Jason S</contributor><contributor> Liu, Jing</contributor><contributor> Souza-Fonseca-Guimaraes, Fernando</contributor><contributor> Hutchinson, Dana S</contributor><contributor> Kolesnik, Tatiana B</contributor><contributor> Nicholson, Sandra E</contributor><contributor> Huntington, Nicholas D</contributor><contributor> Smyth, Mark J</contributor><issued>2015</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.012318883">limited relevance</relevance><identifier type="url" linktype="fulltext">http://arrow.monash.edu.au/hdl/1959.1/1234207</identifier><version id="222759337"><record><header>
        <identifier>monash:163898</identifier>
        <datestamp>2016-05-12T01:41:28.414Z</datestamp>
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      </header><metadata>
      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>DNAM-1 Expression Marks an Alternative Program of NK Cell Maturation</title><creator>Martinet, Ludovic</creator><creator>de Andrade, Lucas</creator><creator>Guillerey, Camille</creator><creator>Lee, Jason</creator><creator>Liu, Jing</creator><creator>Souza-Fonseca-Guimaraes, Fernando</creator><creator>Hutchinson, Dana</creator><creator>Kolesnik, Tatiana</creator><creator>Nicholson, Sandra</creator><creator>Huntington, Nicholas</creator><creator>Smyth, Mark</creator><subject>Biochemistry and cell biology (0601)</subject><publisher>Elsevier Inc</publisher><date>2015</date><type>text</type><type>journal article</type><identifier linktype="fulltext">http://arrow.monash.edu.au/hdl/1959.1/1234207</identifier><identifier>monash:163898</identifier><language>eng</language><relation>Cell Reports [E], vol. 11, p. 85-97</relation><relation>urn:ISSN:2211-1247</relation><relation>http://purl.org/au-research/grants/nhmrc/628623</relation><relation>http://purl.org/au-research/grants/nhmrc/1013667</relation><relation>http://purl.org/au-research/grants/nhmrc/1016647</relation><relation>http://purl.org/au-research/grants/nhmrc/1044392</relation><relation>http://purl.org/au-research/grants/nhmrc/1049407</relation><relation>http://purl.org/au-research/grants/nhmrc/1066770</relation><relation>http://purl.org/au-research/grants/nhmrc/1057852</relation><relation>http://purl.org/au-research/grants/nhmrc/361646</relation><rights>Open access to fulltext</rights><free_to_read /></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2015</issued><holdingsCount>1</holdingsCount></version><version id="234137875"><record><header>
      <identifier>oai:espace.library.uq.edu.au:UQ:355726</identifier>
      <datestamp>2017-11-03T08:27:39Z</datestamp>
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	            <title>DNAM-1 Expression Marks an Alternative Program of NK Cell Maturation</title>
	
		





	





	
	
	
        <bibliographicCitation>
        Martinet, Ludovic, FerrariDeAndrade, Lucas, Guillerey, Camille, Lee, Jason S, Liu, Jing, Souza-Fonseca-Guimaraes, Fernando, Hutchinson, Dana S, Kolesnik, Tatiana B, Nicholson, Sandra E, Huntington, Nicholas D and Smyth, Mark J (2015) DNAM-1 Expression Marks an Alternative Program of NK Cell Maturation. Cell Reports, 11 1: 85-97. doi:10.1016/j.celrep.2015.03.006
    </bibliographicCitation><relation>http://doi.org/10.1016/j.celrep.2015.03.006
    </relation>
    
	
	
	

	
        <type>journal article</type>
        <date>2015-04-01</date>
																        <creator>Martinet, Ludovic</creator>
							        <creator>FerrariDeAndrade, Lucas</creator>
							        <creator>Guillerey, Camille</creator>
							        <creator>Lee, Jason S</creator>
							        <creator>Liu, Jing</creator>
							        <creator>Souza-Fonseca-Guimaraes, Fernando</creator>
							        <creator>Hutchinson, Dana S</creator>
							        <creator>Kolesnik, Tatiana B</creator>
							        <creator>Nicholson, Sandra E</creator>
							        <creator>Huntington, Nicholas D</creator>
							        <creator>Smyth, Mark J</creator>
											
		        
		

		
		

						        	<publisher>Elsevier Inc</publisher>
												        			      			      <language>eng</language>
			      					

		


		        <identifier linktype="notonline">http://espace.library.uq.edu.au/view/UQ:355726</identifier>

		
	      </dc>
	




    </metadata><metadataSource type="nuc">QU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2015-04-01</issued><holdingsCount>1</holdingsCount></version></work><work id="189983873" url="/work/189983873"><troveUrl>http://trove.nla.gov.au/work/189983873</troveUrl><title>IL-21 modulates activation of NKT cells in patients with stage IV malignant melanoma</title><contributor>Coquet, Jonathan M</contributor><contributor> Skak, Kresten</contributor><contributor> Davis, Ian D</contributor><contributor> Smyth, Mark J</contributor><contributor> GODFREY, DALE I</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> funded in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>) </snippet><identifier type="url" linktype="fulltext">http://hdl.handle.net/11343/39665</identifier><version id="209154763"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/39665</identifier>
                <datestamp>2017-02-16T20:44:02Z</datestamp>
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<title>IL-21 modulates activation of NKT cells in patients with stage IV malignant melanoma</title>
<creator>Coquet, Jonathan M.</creator>
<creator>Skak, Kresten</creator>
<creator>Davis, Ian D.</creator>
<creator>Smyth, Mark J.</creator>
<creator>GODFREY, DALE I.</creator>




<abstract>Interleukin-21 (IL-21) is a common γ-chain cytokine produced by T helper and natural killer T (NKT) cells. It has been shown to regulate the response of various lymphocyte subsets including NK, NKT, T and B cells. Owing to its potent anti-tumor function in preclinical studies and its ability to induce cytotoxicity and interferon-γ (IFN-γ) production in NK and CD8 T cells, recombinant IL-21 (rIL-21) was fast-tracked into early-phase clinical trials of patients with various malignancies. In a phase 2a trial of patients with metastatic melanoma, we analyzed the frequency and function of NKT cells in patients receiving rIL-21. NKT cells were present at a low frequency, but their levels were relatively stable in patients administered rIL-21. Unlike our observations in NK and CD8 T cells, rIL-21 appeared to reduce IFN-γ and TNF production by NKT cells, whereas it enhanced IL-4 production. It also modulated the expression of cell surface markers, specifically on CD4− NKT cells. In addition, an increase in CD3+CD56+ NKT-like cells was observed over the course of rIL-21 administration. These results highlight that IL-21 is a potent regulator of NKT cell function in vivo.</abstract>
<description>Published Version</description>
<description>© 2013 Australasian Society for Immunology Inc.</description>
<description>This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons. org/licenses/by-nc-nd/3.0/</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC)</description>
<dateAccepted>2014-06-16T15:51:54Z</dateAccepted>
<available>2014-06-16T15:51:54Z</available>
<created>2014-06-16T15:51:54Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Nature Publishing Group</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
					http://doi.org/10.1038/cti.2013.7</relation>
<isPartOf type="series">Clinical & Translational Immunology</isPartOf>
<bibliographicCitation type="volume">2</bibliographicCitation>
<bibliographicCitation type="issn">2050-0068</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="fulltext">http://hdl.handle.net/11343/39665</identifier>
<subject>NKT</subject><subject>T helper</subject><subject>IL-21</subject><subject>cancer</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="190007413" url="/work/190007413"><troveUrl>http://trove.nla.gov.au/work/190007413</troveUrl><title>CD1d protein structure determines species-selective antigenicity of isoglobotrihexosylceramide (iGb3) to invariant NKT cells</title><contributor>Sanderson, Joseph P</contributor><contributor> Brennan, Patrick J</contributor><contributor> Mansour, Salah</contributor><contributor> Matulis, Gediminas</contributor><contributor> Patel, Onisha</contributor><contributor> Lissin, Nikolai</contributor><contributor> GODFREY, DALE I</contributor><contributor> Kawahara, Kazuyoshi</contributor><contributor> Zähringer, Ulrich</contributor><contributor> ROSSJOHN, JAMIE</contributor><contributor> Brenner, Michael B</contributor><contributor> Gadola, Stephan D</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><version id="209154804"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/39706</identifier>
                <datestamp>2017-02-16T21:01:59Z</datestamp>
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<title>CD1d protein structure determines species-selective antigenicity of isoglobotrihexosylceramide (iGb3) to invariant NKT cells</title>
<creator>Sanderson, Joseph P.</creator>
<creator>Brennan, Patrick J.</creator>
<creator>Mansour, Salah</creator>
<creator>Matulis, Gediminas</creator>
<creator>Patel, Onisha</creator>
<creator>Lissin, Nikolai</creator>
<creator>GODFREY, DALE I.</creator>
<creator>Kawahara, Kazuyoshi</creator>
<creator>Zähringer, Ulrich</creator>
<creator>ROSSJOHN, JAMIE</creator>
<creator>Brenner, Michael B.</creator>
<creator>Gadola, Stephan D.</creator>


























<abstract>Isoglobotrihexosylceramide (iGb3) has been identified as a potent CD1d-presented self-antigen for mouse invariant natural killer T (iNKT) cells. The role of iGb3 in humans remains unresolved, however, as there have been conflicting reports about iGb3-dependent human iNKT-cell activation, and humans lack iGb3 synthase, a key enzyme for iGb3 synthesis. Given the importance of human immune responses, we conducted a human-mouse cross-species analysis of iNKT-cell activation by iGb3-CD1d. Here we show that human and mouse iNKT cells were both able to recognise iGb3 presented by mouse CD1d (mCD1d), but not human CD1d (hCD1d), as iGb3-hCD1d was unable to support cognate interactions with the iNKT-cell TCRs tested in this study. The structural basis for this discrepancy was identified as a single amino acid variation between hCD1d and mCD1d, a glycine-to-tryptophan modification within the α2-helix that prevents flattening of the iGb3 headgroup upon TCR ligation. Mutation of the human residue, Trp153, to the mouse ortholog, Gly155, therefore allowed iGb3-hCD1d to stimulate human iNKT cells. In conclusion, our data indicate that iGb3 is unlikely to be a major antigen in human iNKT-cell biology.</abstract>
<description>Published Version</description>
<description>© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:54:36Z</dateAccepted>
<available>2014-06-16T15:54:36Z</available>
<created>2014-06-16T15:54:36Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Wiley-Blackwell</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1021972</relation>
<relation>
					http://doi.org/10.1002/eji.201242952</relation>
<isPartOf type="series">European Journal of Immunology</isPartOf>
<bibliographicCitation type="volume">43</bibliographicCitation>
<bibliographicCitation type="issue">3</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39706</identifier>
<subject>amino acids</subject><subject>animals</subject><subject>antigen presentation</subject><subject>antigens</subject><subject>CD1d/chemistry</subject><subject>antigens</subject><subject>CD1d/immunology</subject><subject>antigens</subject><subject>CD1d/metabolism</subject><subject>globosides/immunology</subject><subject>globosides/metabolism</subject><subject>humans</subject><subject>lymphocyte activation/immunology</subject><subject>mice</subject><subject>models</subject><subject>molecular</subject><subject>natural killer T-cells/immunology</subject><subject>protein binding</subject><subject>protein conformation</subject><subject>protein interaction domains and motifs</subject><subject>receptors</subject><subject>antigen</subject><subject>T-cell/metabolism</subject><subject>species specificity</subject><subject>trihexosylceramides/immunology</subject><subject>trihexosylceramides/metabolism</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="191549481" url="/work/191549481"><troveUrl>http://trove.nla.gov.au/work/191549481</troveUrl><title>In-vivo stimulation of macaque natural killer T cells with α-galactosylceramide</title><contributor>Fernandez, C. S</contributor><contributor> Jegaskanda, S</contributor><contributor> Godfrey, D. I</contributor><contributor> Kent, S. J</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> funded in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><version id="209154799"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/39701</identifier>
                <datestamp>2017-02-16T20:59:19Z</datestamp>
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<title>In-vivo stimulation of macaque natural killer T cells with α-galactosylceramide</title>
<creator>Fernandez, C. S.</creator>
<creator>Jegaskanda, S.</creator>
<creator>Godfrey, D. I.</creator>
<creator>Kent, S. J.</creator>

















<abstract>Natural killer T cells are a potent mediator of anti-viral immunity in mice, but little is known about the effects of manipulating NKT cells in non-human primates. We evaluated the delivery of the NKT cell ligand, α-galactosylceramide (α-GalCer), in 27 macaques by studying the effects of different dosing (1-100 μg), and delivery modes [directly intravenously (i.v.) or pulsed onto blood or peripheral blood mononuclear cells]. We found that peripheral NKT cells were depleted transiently from the periphery following α-GalCer administration across all delivery modes, particularly in doses of ≥10 μg. Furthermore, NKT cell numbers frequently remained depressed at i.v. α-GalCer doses of >10 μg. Levels of cytokine expression were also not enhanced after α-GalCer delivery to macaques. To evaluate the effects of α-GalCer administration on anti-viral immunity, we administered α-GalCer either together with live attenuated influenza virus infection or prior to simian immunodeficiency virus (SIV) infection of two macaques. There was no clear enhancement of influenza-specific T or B cell immunity following α-GalCer delivery. Further, there was no modulation of pathogenic SIVmac251 infection following α-GalCer delivery to a further two macaques in a pilot study. Accordingly, although macaque peripheral NKT cells are modulated by α-GalCer in vivo, at least for the dosing regimens tested in this study, this does not appear to have a significant impact on anti-viral immunity in macaque models.</abstract>
<description>Published Version</description>
<description>© 2013 British Society for Immunology</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:54:16Z</dateAccepted>
<available>2014-06-16T15:54:16Z</available>
<created>2014-06-16T15:54:16Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Wiley-Blackwell</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/454569</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/454309</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/508937</relation>
<relation>
					http://doi.org/10.1111/cei.12132</relation>
<isPartOf type="series">Clinical and Experimental Immunology</isPartOf>
<bibliographicCitation type="volume">173</bibliographicCitation>
<bibliographicCitation type="issue">3</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39701</identifier>
<subject>adjuvants</subject><subject>immunologic/administration & dosage</subject><subject>adjuvants</subject><subject>immunologic/pharmacology</subject><subject>animals</subject><subject>galactosylceramides/administration & dosage</subject><subject>galactosylceramides/pharmacology</subject><subject>lymphocyte activation/drug effects</subject><subject>lymphocyte activation/immunology</subject><subject>lymphocyte count</subject><subject>Macaca nemestrina</subject><subject>monkey diseases/immunology</subject><subject>natural killer T-cells/drug effects</subject><subject>natural killer T-cells/immunology</subject><subject>natural killer T-cells/metabolism</subject><subject>simian acquired immunodeficiency syndrome/immunology</subject><subject>simian immunodeficiency virus/immunology</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="182262342" url="/work/182262342"><troveUrl>http://trove.nla.gov.au/work/182262342</troveUrl><title>A conserved human T cell population targets mycobacterial antigens presented by CD1b</title><contributor>Van Rhijn, Ildiko</contributor><contributor> Kasmar, Anne</contributor><contributor> de Jong, Annemieke</contributor><contributor> Gras, Stephanie</contributor><contributor> Bhati, Mugdha</contributor><contributor> Doorenspleet, Marieke E</contributor><contributor> de Vries, Niek</contributor><contributor> Godfrey, Dale I</contributor><contributor> Altman, John D</contributor><contributor> de Jager, Wilco</contributor><contributor> Rossjohn, Jamie</contributor><contributor> Moody, D. Branch</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><type>Article/Report</type><isPartOf url="/work/7313225">Nature Immunology</isPartOf><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><identifier type="url" linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/938682</identifier><version id="208511989 209154790"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/39692</identifier>
                <datestamp>2017-02-16T20:56:30Z</datestamp>
                <setSpec>com_11343_225</setSpec>
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            </header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>A conserved human T cell population targets mycobacterial antigens presented by CD1b</title>
<creator>Van Rhijn, Ildiko</creator>
<creator>Kasmar, Anne</creator>
<creator>de Jong, Annemieke</creator>
<creator>Gras, Stephanie</creator>
<creator>Bhati, Mugdha</creator>
<creator>Doorenspleet, Marieke E.</creator>
<creator>de Vries, Niek</creator>
<creator>GODFREY, DALE I.</creator>
<creator>Altman, John D.</creator>
<creator>de Jager, Wilco</creator>
<creator>ROSSJOHN, JAMIE</creator>
<creator>Moody, D. Branch</creator>










<abstract>Human T cell antigen receptors (TCRs) pair in millions of combinations to create complex and unique T cell repertoires for each person. Through the use of tetramers to analyze TCRs reactive to the antigen-presenting molecule CD1b, we detected T cells with highly stereotyped TCR alpha-chains present among genetically unrelated patients with tuberculosis. The germline-encoded, mycolyl lipid-reactive (GEM) TCRs had an alpha-chain bearing the variable (V) region TRAV1-2 rearranged to the joining (J) region TRAJ9 with few nontemplated (N)-region additions. Analysis of TCRs by high-throughput sequencing, binding and crystallography showed linkage of TCR alpha sequence motifs to high-affinity recognition of antigen. Thus, the CD1-reactive TCR repertoire is composed of at least two compartments: high-affinity GEM TCRs, and more-diverse TCRs with low affinity for CD1b-lipid complexes. We found high interdonor conservation of TCRs that probably resulted from selection by a nonpolymorphic antigen-presenting molecule and an immunodominant antigen.</abstract>
<description>Published Version</description>
<description>© 2013 Nature America, Inc. All rights reserved.</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:53:45Z</dateAccepted>
<available>2014-06-16T15:53:45Z</available>
<created>2014-06-16T15:53:45Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Nature Publishing Group</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
					http://doi.org/10.1038/ni.2630</relation>
<isPartOf type="series">Nature Immunology</isPartOf>
<bibliographicCitation type="volume">14</bibliographicCitation>
<bibliographicCitation type="issue">7</bibliographicCitation>
<bibliographicCitation type="issn">1529-2908</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39692</identifier>
<subject>tuberculosis infection</subject><subject>lipid antigens</subject><subject>alpha-chain</subject><subject>mait cells</subject><subject>receptor</subject><subject>recognition</subject><subject>responses</subject><subject>expression</subject><subject>lymphocytes</subject><subject>memory</subject></qualifieddc>
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        <identifier>monash:122341</identifier>
        <datestamp>2015-02-03T03:11:11.426Z</datestamp>
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      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>A conserved human T cell population targets mycobacterial antigens presented by CD1b</title><creator>Van Rhijn, Ildiko</creator><creator>Kasmar, Anne</creator><creator>de Jong, Annemieke</creator><creator>Gras, Stephanie</creator><creator>Bhati, Mugdha</creator><creator>Doorenspleet, Marieke</creator><creator>de Vries, Nick</creator><creator>Godfrey, Dale</creator><creator>Altman, John</creator><creator>de Jager, Wilco</creator><creator>Rossjohn, Jamie</creator><creator>Moody, D</creator><subject>Immunology (1107)</subject><publisher>Nature Publishing Group</publisher><date>2013</date><type>text</type><type>journal article</type><identifier linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/938682</identifier><identifier>monash:122341</identifier><language>eng</language><relation>Nature Immunology [P], vol. 14, no. 7, p. 706-713</relation><relation>urn:ISSN:15292908</relation><rights>Subscription access to fulltext</rights></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>2</holdingsCount></version><version id="198574398"><record><identifier type="galeAccessionNumber">336175876</identifier><bibliographicCitation type="yearIssued">2013</bibliographicCitation><bibliographicCitation type="dateIssued">July</bibliographicCitation><bibliographicCitation type="volume">14</bibliographicCitation><bibliographicCitation type="issue">7</bibliographicCitation><issued type="dcterms:W3CDTF">2013-07-01</issued><title>A conserved human T cell population targets mycobacterial
antigens presented by CD1b.(Report)</title><language>English</language><alternative>A conserved human T cell population targets
mycobacterial antigens presented by CD1b.</alternative><creator>Van Rhijn, Ildiko</creator><creator>Kasmar, Anne</creator><creator>de Jong, Annemieke</creator><creator>Gras, Stephanie</creator><creator>Bhati, Mugdha</creator><creator>Doorenspleet, Marieke E.</creator><creator>de Vries, Niek</creator><creator>Godfrey, Dale I.</creator><creator>Altman, John D.</creator><creator>de Jager, Wilco</creator><creator>Rossjohn, Jamie</creator><creator>Moody, D. Branch</creator><description type="byline">Van Rhijn, Ildiko^Kasmar, Anne^de Jong, Annemieke^Gras,
Stephanie^Bhati, Mugdha^Doorenspleet, Marieke E.^ de Vries,
Niek^Godfrey, Dale I.^Altman, John D.^de Jager, Wilco^Rossjohn,
Jamie^Moody, D. Branch</description><bibliographicCitation type="pagination">706(10)</bibliographicCitation><subject code="2836" type="SIC">Biological products exc. diagnostic</subject><subject>Antigen receptors, T cell -- Physiological aspects</subject><subject>Antigen receptors, T cell -- Genetic aspects</subject><subject>Antigen receptors, T cell -- Research</subject><subject>T cells -- Physiological aspects</subject><subject>T cells -- Research</subject><subject>Antigens -- Identification and classification</subject><subject>Antigens -- Research</subject><subject>Antigens -- Reports</subject><subject>T cells -- Receptors</subject><subject>T cells -- Genetic aspects</subject><type>Report</type><subject>T cell antigen receptors -- Physiological aspects</subject><subject>T cell antigen receptors -- Genetic aspects</subject><subject>T cell antigen receptors -- Research</subject><subject>T cells -- Physiological aspects</subject><subject>T cells -- Research</subject><subject>Antigens -- Identification and classification</subject><subject>Antigens -- Research</subject><subject>Antigens -- Reports</subject><subject code="310" type="eventCode">Science & research</subject><subject type="topicalScope">Physiological aspects</subject><subject type="topicalScope">Genetic aspects</subject><subject type="topicalScope">Research</subject><subject type="topicalScope">Identification and classification</subject><subject type="topicalScope">Reports</subject><isPartOf code="GALE2IHQ" type="publication">Nature Immunology</isPartOf><publisher>Nature Publishing Group</publisher><audience>Academic</audience><medium type="publication">Magazine/Journal article</medium><subject>Health</subject><bibliographicCitation type="issn">1529-2908</bibliographicCitation><rights type="metadata">Copyright 2013 Gale, Cengage Learning.  All rights
reserved.</rights><metadataSource>GALE</metadataSource></record><type>Article</type><type>Article/Report</type><issued>2013-07-01</issued><holdingsCount>0</holdingsCount></version></work><work id="190007414" url="/work/190007414"><troveUrl>http://trove.nla.gov.au/work/190007414</troveUrl><title>Ex-vivo analysis of human natural killer T cells demonstrates heterogeneity between tissues and within established CD4(+) and CD4(-) subsets</title><contributor>Chan, A. C</contributor><contributor> Leeansyah, E</contributor><contributor> Cochrane, A</contributor><contributor> d'Udekem d'Acoz, Y</contributor><contributor> Mittag, D</contributor><contributor> Harrison, L. C</contributor><contributor> Godfrey, D. I</contributor><contributor> Berzins, S. P</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><version id="209154803"><record><header>
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                <datestamp>2017-02-16T21:01:59Z</datestamp>
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<title>Ex-vivo analysis of human natural killer T cells demonstrates heterogeneity between tissues and within established CD4(+) and CD4(-) subsets</title>
<creator>Chan, A. C.</creator>
<creator>Leeansyah, E.</creator>
<creator>Cochrane, A.</creator>
<creator>d'Udekem d'Acoz, Y.</creator>
<creator>Mittag, D.</creator>
<creator>Harrison, L. C.</creator>
<creator>Godfrey, D. I.</creator>
<creator>Berzins, S. P.</creator>
























<abstract>Our understanding of human type 1 natural killer T (NKT) cells has been heavily dependent on studies of cells from peripheral blood. These have identified two functionally distinct subsets defined by expression of CD4, although it is widely believed that this underestimates the true number of subsets. Two recent studies supporting this view have provided more detail about diversity of the human NKT cells, but relied on analysis of NKT cells from human blood that had been expanded in vitro prior to analysis. In this study we extend those findings by assessing the heterogeneity of CD4(+) and CD4(-) human NKT cell subsets from peripheral blood, cord blood, thymus and spleen without prior expansion ex vivo, and identifying for the first time cytokines expressed by human NKT cells from spleen and thymus. Our comparative analysis reveals highly heterogeneous expression of surface antigens by CD4(+) and CD4(-) NKT cell subsets and identifies several antigens whose differential expression correlates with the cytokine response. Collectively, our findings reveal that the common classification of NKT cells into CD4(+) and CD4(-) subsets fails to reflect the diversity of this lineage, and that more studies are needed to establish the functional significance of the antigen expression patterns and tissue residency of human NKT cells.</abstract>
<description>Published Version</description>
<description>© 2012 British Society for Immunology</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:54:29Z</dateAccepted>
<available>2014-06-16T15:54:29Z</available>
<created>2014-06-16T15:54:29Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Wiley-Blackwell</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
					http://doi.org/10.1111/cei.12045</relation>
<isPartOf type="series">Clinical and Experimental Immunology</isPartOf>
<bibliographicCitation type="volume">172</bibliographicCitation>
<bibliographicCitation type="issue">1</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39705</identifier>
<subject>antigens</subject><subject>CD4/genetics</subject><subject>antigens</subject><subject>CD4/immunology</subject><subject>CD4-positive T-lymphocytes/cytology</subject><subject>CD4-positive T-lymphocytes/immunology</subject><subject>cells</subject><subject>cultured</subject><subject>cytokines/biosynthesis</subject><subject>cytokines/immunology</subject><subject>fetal blood/cytology</subject><subject>fetal blood/immunology</subject><subject>fetus</subject><subject>gene expression</subject><subject>genetic heterogeneity</subject><subject>humans</subject><subject>immunophenotyping</subject><subject>natural killer T-cells/cytology</subject><subject>natural killer T-cells/immunology</subject><subject>organ specificity</subject><subject>T-lymphocyte subsets/cytology</subject><subject>T-lymphocyte subsets/immunology</subject><subject>thymus gland/cytology</subject><subject>thymus gland/immunology</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="191549478" url="/work/191549478"><troveUrl>http://trove.nla.gov.au/work/191549478</troveUrl><title>Ex-vivo α-galactosylceramide activation of NKT cells in humans and macaques</title><contributor>Fernandez, Caroline S</contributor><contributor> CAMERON, GARTH</contributor><contributor> GODFREY, DALE I</contributor><contributor> Kent, Stephen J</contributor><issued>2012</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> and Medical <b>Research</b> Council (<b>NHMRC</b>). </snippet><version id="209154778"><record><header>
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<title>Ex-vivo α-galactosylceramide activation of NKT cells in humans and macaques</title>
<creator>Fernandez, Caroline S.</creator>
<creator>CAMERON, GARTH</creator>
<creator>GODFREY, DALE I.</creator>
<creator>Kent, Stephen J.</creator>










<abstract>NKT cells are key mediators of antiviral and anticancer immunity. Experiments in mice have demonstrated that activation of NKT cells in vivo induces the expression of multiple effector molecules critical to successful immunity. Human clinical trials have shown similar responses, although in vivo activation of NKT cells in humans or primate models are far more limited in number and scope. Measuring ex vivo activation of NKT cells by the CD1d-restricted glycolipid ligand alpha-Galactosylceramide (alpha-GalCer) through cytokine expression profiles is a useful marker of NKT cell function, but for reasons that are unclear, this approach does not appear to work as well in humans and non-human primate macaque models in comparison to mice. We performed a series of experiments on human and macaque (Macaca nemestrina) fresh whole blood samples to define optimal conditions to detect NKT cell cytokine (TNF, IFN gamma, IL-2) and degranulation marker (CD107a) expression by flow cytometry. We found that conditions previously described for mouse splenocyte NKT cell activation were suboptimal on human or macaque blood NKT cells. In contrast, a 6 h incubation with brefeldin A added for the last 4 h, in a 96-well plate based assay, and using an alpha-GalCer concentration of 1 mu g/ml were optimal methods to stimulate NKT cells in fresh blood from both humans and macaques. Unexpectedly, we noted that blood NKT cells from macaques infected with SIV were more readily activated by alpha-GalCer than NKT cells from uninfected macaques, suggesting that SIV infection may have primed the NKT cells. In conclusion, we describe optimized methods for the ex vivo antigen-specific activation of human and macaque blood NKT cells. These assays should be useful in monitoring NKT cells in disease and in immunotherapy studies.</abstract>
<description>Published Version</description>
<description>© 2012 Elsevier B.V.</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:52:51Z</dateAccepted>
<available>2014-06-16T15:52:51Z</available>
<created>2014-06-16T15:52:51Z</created>
<issued>2012</issued>
<type>journal article</type>
<publisher>Elsevier</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
					http://doi.org/10.1016/j.jim.2012.05.019</relation>
<isPartOf type="series">Journal of Immunological Methods</isPartOf>
<bibliographicCitation type="volume">382</bibliographicCitation>
<bibliographicCitation type="issue">1-2</bibliographicCitation>
<bibliographicCitation type="issn">0022-1759</bibliographicCitation>
<bibliographicCitation type="yearIssued">2012</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39680</identifier>
<subject>killer T-cells</subject><subject>antigen-presenting cells</subject><subject>immunodeficiency-virus</subject><subject>brefeldin-a</subject><subject>in-vivo</subject><subject>phase-i</subject><subject>protective immunity</subject><subject>dendritic cells</subject><subject>CD1d tetramers</subject><subject>recurrent head</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2012</issued><holdingsCount>1</holdingsCount></version></work><work id="204614337" url="/work/204614337"><troveUrl>http://trove.nla.gov.au/work/204614337</troveUrl><title>Antigen Specificity of Type I NKT Cells Is Governed by TCR beta-Chain Diversity</title><contributor>Cameron, Garth</contributor><contributor> Pellicci, Daniel</contributor><contributor> Uldrich, Adam</contributor><contributor> Besra, Gurdyal</contributor><contributor> Illarionov, Petr</contributor><contributor> Williams, Spencer</contributor><contributor> La Gruta, Nicole</contributor><contributor> Rossjohn, Jamie</contributor><contributor> Godfrey, Dale</contributor><issued>2015</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.0098551065">limited relevance</relevance><identifier type="url" linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/1244422</identifier><version id="224609232"><record><header>
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      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>Antigen Specificity of Type I NKT Cells Is Governed by TCR beta-Chain Diversity</title><creator>Cameron, Garth</creator><creator>Pellicci, Daniel</creator><creator>Uldrich, Adam</creator><creator>Besra, Gurdyal</creator><creator>Illarionov, Petr</creator><creator>Williams, Spencer</creator><creator>La Gruta, Nicole</creator><creator>Rossjohn, Jamie</creator><creator>Godfrey, Dale</creator><subject>Immunology (1107)</subject><publisher>American Association of Immunologists</publisher><date>2015</date><type>text</type><type>journal article</type><identifier linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/1244422</identifier><identifier>monash:166238</identifier><language>eng</language><relation>Journal Of Immunology [P], vol. 195, no. 10, p. 4604-4614</relation><relation>urn:ISSN:0022-1767</relation></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2015</issued><holdingsCount>1</holdingsCount></version><version id="248945603"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/168274</identifier>
                <datestamp>2017-06-26T05:20:58Z</datestamp>
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<title>Antigen Specificity of Type I NKT Cells Is Governed by TCR beta-Chain Diversity</title>
<creator>LA GRUTA, NICOLE</creator>
<creator>PELLICCI, DANIEL</creator>
<creator>GODFREY, DALE</creator>
<creator>ROSSJOHN, JAMIE</creator>
<creator>ULDRICH, ADAM</creator>
<creator>WILLIAMS, SPENCER</creator>
<abstract>NKT cells recognize lipid-based Ags presented by CD1d. Type I NKT cells are often referred to as invariant owing to their mostly invariant TCR α-chain usage (Vα14-Jα18 in mice, Vα24-Jα18 in humans). However, these cells have diverse TCR β-chains, including Vβ8, Vβ7, and Vβ2 in mice and Vβ11 in humans, joined to a range of TCR Dβ and Jβ genes. In this study, we demonstrate that TCR β-chain composition can dramatically influence lipid Ag recognition in an Ag-dependent manner. Namely, the glycolipids α-glucosylceramide and isoglobotrihexosylceramide were preferentially recognized by Vβ7(+) NKT cells from mice, whereas the α-galactosylceramide analog OCH, with a truncated sphingosine chain, was preferentially recognized by Vβ8(+) NKT cells from mice. We show that the influence of the TCR β-chain is due to a combination of Vβ-, Jβ-, and CDR3β-encoded residues and that these TCRs can recapitulate the selective Ag reactivity in TCR-transduced cell lines. Similar observations were made with human NKT cells where different CDR3β-encoded residues determined Ag preference. These findings indicate that NKT TCR β-chain diversity results in differential and nonhierarchical Ag recognition by these cells, which implies that some Ags can preferentially activate type I NKT cell subsets.</abstract>
<dateAccepted>2017-06-16T01:42:33Z</dateAccepted>
<available>2017-06-16T01:42:33Z</available>
<created>2017-06-16T01:42:33Z</created>
<issued>2015-11-15</issued>
<type>journal article</type>
<publisher>AMER ASSOC IMMUNOLOGISTS</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1021972</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1046333</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1054431</relation>
<relation>
					http://purl.org/au-research/grants/ARC/FT140100278</relation>
<relation>
					http://purl.org/au-research/grants/ARC/FT140100278</relation>


<relation>
					http://orcid.org/0000-0002-3009-5472</relation>

<relation>
					http://orcid.org/0000-0002-6350-5976</relation>
<relation>
					http://orcid.org/0000-0001-6341-4364</relation>
<relation>
					http://doi.org/10.4049/jimmunol.1501222</relation>
<isPartOf type="series">JOURNAL OF IMMUNOLOGY</isPartOf>
<bibliographicCitation type="volume">195</bibliographicCitation>
<bibliographicCitation type="issue">10</bibliographicCitation>
<bibliographicCitation type="issn">0022-1767</bibliographicCitation>
<bibliographicCitation type="yearIssued">2015-11-15</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/168274</identifier>
</qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2015-11-15</issued><holdingsCount>1</holdingsCount></version></work><work id="189916855" url="/work/189916855"><troveUrl>http://trove.nla.gov.au/work/189916855</troveUrl><title>DOCK8 is critical for the survival and function of NKT cells</title><contributor>Crawford, Greg</contributor><contributor> Enders, Anselm</contributor><contributor> Gileadi, Uzi</contributor><contributor> Stankovic, Sanda</contributor><contributor> Zhang, Qian</contributor><contributor> Lambe, Teresa</contributor><contributor> Crockford, Tanya L</contributor><contributor> Lockstone, Helen E</contributor><contributor> Freeman, Alexandra</contributor><contributor> Arkwright, Peter D</contributor><contributor> Smart, Joanne M</contributor><contributor> Ma, Cindy S</contributor><contributor> Tangye, Stuart G</contributor><contributor> Goodnow, Christopher C</contributor><contributor> Cerundolo, Vincenzo</contributor><contributor> Godfrey, Dale I</contributor><contributor> Su, Helen C</contributor><contributor> Randall, Katrina L</contributor><contributor> Cornall, Richard J</contributor><issued>2013-2015</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>3</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> <b>NHMRC</b></snippet><identifier type="url" linktype="unknown">http://hdl.handle.net/1885/11345</identifier><version id="206642484 244994375"><record><header><identifier>oai:openresearch-repository.anu.edu.au:1885/11345</identifier><datestamp>2017-04-06T04:19:07Z</datestamp><setSpec>com_1885_9051</setSpec><setSpec>com_1885_1</setSpec><setSpec>col_1885_26</setSpec></header><metadata><dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
<title>DOCK8 is critical for the survival and function of NKT cells</title>
<creator>Crawford, Greg</creator>
<creator>Enders, Anselm</creator>
<creator>Gileadi, Uzi</creator>
<creator>Stankovic, Sanda</creator>
<creator>Zhang, Qian</creator>
<creator>Lambe, Teresa</creator>
<creator>Crockford, Tanya L</creator>
<creator>Lockstone, Helen E</creator>
<creator>Freeman, Alexandra</creator>
<creator>Arkwright, Peter D</creator>
<creator>Smart, Joanne M</creator>
<creator>Ma, Cindy S</creator>
<creator>Tangye, Stuart G</creator>
<creator>Goodnow, Christopher C</creator>
<creator>Cerundolo, Vincenzo</creator>
<creator>Godfrey, Dale I</creator>
<creator>Su, Helen C</creator>
<creator>Randall, Katrina L</creator>
<creator>Cornall, Richard J</creator>
<subject>immunodeficiency syndrome</subject>
<subject>cytokinesis 8</subject>
<subject>DOCK 8</subject>
<subject>NKT</subject>
<description>Patients with the dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome suffer from recurrent viral and bacterial infections, hyper–immunoglobulin E levels, eczema, and greater susceptibility to cancer. Because natural killer T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency. Using a mouse model, we found that DOCK8 deficiency resulted in impaired NKT cell development, principally affecting the formation and survival of long-lived, differentiated NKT cells. In the thymus, DOCK8-deficient mice lack a terminally differentiated subset of NK1.1+ NKT cells expressing the integrin CD103, whereas in the liver, DOCK8-deficient NKT cells express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte function-associated antigen 1. Although the initial NKT cell response to antigen is intact in the absence of DOCK8, their ongoing proliferative and cytokine responses are impaired. Importantly, a similar defect in NKT cell numbers was detected in DOCK8-deficient humans, highlighting the relevance of the mouse model. In conclusion, our data demonstrate that DOCK8 is required for the development and survival of mature NKT cells, consistent with the idea that DOCK8 mediates survival signals within a specialized niche. Accordingly, impaired NKT cell numbers and function are likely to contribute to the susceptibility of DOCK8-deficient patients to recurrent infections and malignant disease.</description>
<description>This work was supported by the Medical Research Council, National Institute for Health Research Biomedical Research Centre Program, National Institutes of Medical Research, Australian National Health and Medical Research Council (NHMRC), and the Intramural Research Program of the National Institutes of Health, National Institute of Allergy and Infectious Diseases. The authors acknowledge the following personal awards: Medical Research Council Centenary Early Career Award (to G.C.), NHMRC Career Development Fellowship (to A.E.), NHMRC Senior Principal Research Fellowship (to D.I.G.), NHMRC Career Development Fellowship (to C.S.M.), NHMRC grant GNT1022922 (to K.L.R.), and NHMRC Principal Research Fellowship (to S.G.T.).</description>
<date>2014-02-17T01:38:12Z</date>
<date>2014-02-17T01:38:12Z</date>
<date>2013-09-19</date>
<date>2015-12-09T07:48:04Z</date>
<type>journal article</type>
<identifier>0006-4971</identifier>
<identifier linktype="unknown">http://hdl.handle.net/1885/11345</identifier>
<identifier>10.1182/blood-2013-02-482331</identifier>
<relation>http://purl.org/au-research/grants/nhmrc/1022922</relation>
<rights>http://www.sherpa.ac.uk/romeo/issn/0006-4971/author cannot archive pre-print (ie pre-refereeing); author can archive post-print (ie final draft post-refereeing); author cannot archive publisher's version/PDF</rights>
<format>10 pages</format>
<publisher>American Society of Hematology</publisher>
<source>Blood 122.12 (2013):2052-61</source>
</dc>
</metadata><metadataSource type="nuc">ANU:IR</metadataSource></record><record><header><identifier>oai:digitalcollections.anu.edu.au:1885/11345</identifier><datestamp>2015-12-09T07:48:04Z</datestamp><setSpec>com_1885_9051</setSpec><setSpec>com_1885_1</setSpec><setSpec>col_1885_26</setSpec></header><metadata><dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
<title>DOCK8 is critical for the survival and function of NKT cells</title>
<creator>Crawford, Greg</creator>
<creator>Enders, Anselm</creator>
<creator>Gileadi, Uzi</creator>
<creator>Stankovic, Sanda</creator>
<creator>Zhang, Qian</creator>
<creator>Lambe, Teresa</creator>
<creator>Crockford, Tanya L</creator>
<creator>Lockstone, Helen E</creator>
<creator>Freeman, Alexandra</creator>
<creator>Arkwright, Peter D</creator>
<creator>Smart, Joanne M</creator>
<creator>Ma, Cindy S</creator>
<creator>Tangye, Stuart G</creator>
<creator>Goodnow, Christopher C</creator>
<creator>Cerundolo, Vincenzo</creator>
<creator>Godfrey, Dale I</creator>
<creator>Su, Helen C</creator>
<creator>Randall, Katrina L</creator>
<creator>Cornall, Richard J</creator>
<subject>immunodeficiency syndrome</subject>
<subject>cytokinesis 8</subject>
<subject>DOCK 8</subject>
<subject>NKT</subject>
<description>Patients with the dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome suffer from recurrent viral and bacterial infections, hyper–immunoglobulin E levels, eczema, and greater susceptibility to cancer. Because natural killer T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency. Using a mouse model, we found that DOCK8 deficiency resulted in impaired NKT cell development, principally affecting the formation and survival of long-lived, differentiated NKT cells. In the thymus, DOCK8-deficient mice lack a terminally differentiated subset of NK1.1+ NKT cells expressing the integrin CD103, whereas in the liver, DOCK8-deficient NKT cells express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte function-associated antigen 1. Although the initial NKT cell response to antigen is intact in the absence of DOCK8, their ongoing proliferative and cytokine responses are impaired. Importantly, a similar defect in NKT cell numbers was detected in DOCK8-deficient humans, highlighting the relevance of the mouse model. In conclusion, our data demonstrate that DOCK8 is required for the development and survival of mature NKT cells, consistent with the idea that DOCK8 mediates survival signals within a specialized niche. Accordingly, impaired NKT cell numbers and function are likely to contribute to the susceptibility of DOCK8-deficient patients to recurrent infections and malignant disease.</description>
<description>This work was supported by the Medical Research Council, National Institute for Health Research Biomedical Research Centre Program, National Institutes of Medical Research, Australian National Health and Medical Research Council (NHMRC), and the Intramural Research Program of the National Institutes of Health, National Institute of Allergy and Infectious Diseases. The authors acknowledge the following personal awards: Medical Research Council Centenary Early Career Award (to G.C.), NHMRC Career Development Fellowship (to A.E.), NHMRC Senior Principal Research Fellowship (to D.I.G.), NHMRC Career Development Fellowship (to C.S.M.), NHMRC grant GNT1022922 (to K.L.R.), and NHMRC Principal Research Fellowship (to S.G.T.).</description>
<date>2014-02-17T01:38:12Z</date>
<date>2014-02-17T01:38:12Z</date>
<date>2013-09-19</date>
<date>2015-12-09T07:48:04Z</date>
<type>journal article</type>
<identifier>0006-4971</identifier>
<identifier linktype="unknown">http://hdl.handle.net/1885/11345</identifier>
<relation>http://purl.org/au-research/grants/nhmrc/1022922</relation>
<rights>http://www.sherpa.ac.uk/romeo/issn/0006-4971/author cannot archive pre-print (ie pre-refereeing); author can archive post-print (ie final draft post-refereeing); author cannot archive publisher's version/PDF</rights>
<format>10 pages</format>
<publisher>American Society of Hematology</publisher>
<source>Blood 122.12 (2013):2052-61</source>
</dc>
</metadata><metadataSource type="nuc">ANU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2014</issued><issued>2013</issued><issued>2015</issued><holdingsCount>1</holdingsCount></version><version id="249741980"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/190809</identifier>
                <datestamp>2017-07-17T04:52:25Z</datestamp>
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<title>DOCK8 is critical for the survival and function of NKT cells</title>
<creator>GODFREY, DALE</creator>
<creator>STANKOVIC, SANDA</creator>
<abstract>Patients with the dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome suffer from recurrent viral and bacterial infections, hyper-immunoglobulin E levels, eczema, and greater susceptibility to cancer. Because natural killer T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency. Using a mouse model, we found that DOCK8 deficiency resulted in impaired NKT cell development, principally affecting the formation and survival of long-lived, differentiated NKT cells. In the thymus, DOCK8-deficient mice lack a terminally differentiated subset of NK1.1(+) NKT cells expressing the integrin CD103, whereas in the liver, DOCK8-deficient NKT cells express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte function-associated antigen 1. Although the initial NKT cell response to antigen is intact in the absence of DOCK8, their ongoing proliferative and cytokine responses are impaired. Importantly, a similar defect in NKT cell numbers was detected in DOCK8-deficient humans, highlighting the relevance of the mouse model. In conclusion, our data demonstrate that DOCK8 is required for the development and survival of mature NKT cells, consistent with the idea that DOCK8 mediates survival signals within a specialized niche. Accordingly, impaired NKT cell numbers and function are likely to contribute to the susceptibility of DOCK8-deficient patients to recurrent infections and malignant disease.</abstract>
<dateAccepted>2017-07-07T04:37:59Z</dateAccepted>
<available>2017-07-07T04:37:59Z</available>
<created>2017-07-07T04:37:59Z</created>
<issued>2013-09-19</issued>
<type>journal article</type>
<publisher>AMER SOC HEMATOLOGY</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
					http://orcid.org/0000-0002-3009-5472</relation>

<relation>
					http://doi.org/10.1182/blood-2013-02-482331</relation>
<isPartOf type="series">BLOOD</isPartOf>
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<bibliographicCitation type="issue">12</bibliographicCitation>
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<bibliographicCitation type="yearIssued">2013-09-19</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/190809</identifier>
</qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013-09-19</issued><holdingsCount>1</holdingsCount></version><version id="209154754"><record><header>
                <identifier>oai:minerva-access.unimelb.edu.au:11343/39656</identifier>
                <datestamp>2017-02-16T20:40:51Z</datestamp>
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<title>DOCK8 is critical for the survival and function of NKT cells</title>
<creator>Crawford, Greg</creator>
<creator>Enders, Anselm</creator>
<creator>Gileadi, Uzi</creator>
<creator>STANKOVIC, SANDA</creator>
<creator>Zhang, Qian</creator>
<creator>Lambe, Teresa</creator>
<creator>Crockford, Tanya L.</creator>
<creator>Lockstone. Helen E.</creator>
<creator>Freeman, Alexandra</creator>
<creator>Arkwright, Peter D.</creator>
<creator>Smart, Joanne M.</creator>
<creator>Ma, Cindy S.</creator>
<creator>Tangye, Stuart G.</creator>
<creator>Goodnow, Christopher C.</creator>
<creator>Cerundolo, Vincenzo</creator>
<creator>GODFREY, DALE I.</creator>
<creator>Su, Helen C.</creator>
<creator>Randall, Katrina L.</creator>
<creator>Cornall, Richard J.</creator>










<abstract>Patients with the dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome suffer from recurrent viral and bacterial infections, hyper-immunoglobulin E levels, eczema, and greater susceptibility to cancer. Because natural killer T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency. Using a mouse model, we found that DOCK8 deficiency resulted in impaired NKT cell development, principally affecting the formation and survival of long-lived, differentiated NKT cells. In the thymus, DOCK8-deficient mice lack a terminally differentiated subset of NK1.1 1 NKT cells expressing the integrin CD103, whereas in the liver, DOCK8-deficient NKT cells express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte function-associated antigen 1. Although the initial NKT cell response to antigen is intact in the absence of DOCK8, their ongoing proliferative and cytokine responses are impaired. Importantly, a similar defect in NKT cell numbers was detected in DOCK8-deficient humans, highlighting the relevance of the mouse model. In conclusion, our data demonstrate that DOCK8 is required for the development and survival of mature NKT cells, consistent with the idea that DOCK8 mediates survival signals within a specialized niche. Accordingly, impaired NKT cell numbers and function are likely to contribute to the susceptibility of DOCK8-deficient patients to recurrent infections and malignant disease.</abstract>
<description>Published Version</description>
<description>Copyright © 2014 by American Society of Hematology</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:51:21Z</dateAccepted>
<available>2014-06-16T15:51:21Z</available>
<created>2014-06-16T15:51:21Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>American Society of Hematology</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/1020770</relation>
<isPartOf type="series">Blood</isPartOf>
<bibliographicCitation type="volume">122</bibliographicCitation>
<bibliographicCitation type="issue">12</bibliographicCitation>
<bibliographicCitation type="issn">0006-4971</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39656</identifier>
<subject>killer T-cells</subject><subject>germinal center formation</subject><subject>Aldrich syndrome protein</subject><subject>terminal maturation</subject><subject>immune-responses</subject><subject>in-vivo</subject><subject>homeostasis</subject><subject>deficiency</subject><subject>mutations</subject><subject>sap</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="189983875" url="/work/189983875"><troveUrl>http://trove.nla.gov.au/work/189983875</troveUrl><title>Nfil3 is a glucocorticoid-regulated gene required for glucocorticoid-induced apoptosis in male murine T cells</title><contributor>Carey, Kirstyn T</contributor><contributor> Tan, Kheng H</contributor><contributor> Ng, Judy</contributor><contributor> Liddicoat, Douglas R</contributor><contributor> GODFREY, DALE I</contributor><contributor> Cole, Timothy J</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>1</holdingsCount><versionCount>1</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> in this collection have been funded in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>) </snippet><version id="209154761"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/39663</identifier><datestamp>2017-07-28T11:07:44Z</datestamp><setSpec>com_11343_225</setSpec><setSpec>com_11343_164</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_226</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>Nfil3 is a glucocorticoid-regulated gene required for glucocorticoid-induced apoptosis in male murine T cells</title>
<creator>Carey, Kirstyn T.</creator>
<creator>Tan, Kheng H.</creator>
<creator>Ng, Judy</creator>
<creator>Liddicoat, Douglas R.</creator>
<creator>GODFREY, DALE I.</creator>
<creator>Cole, Timothy J.</creator>















<abstract>Glucocorticoids (GCs) have essential roles in the regulation of development, integrated metabolism, and immune and neurological responses, and act primarily via the glucocorticoid receptor (GR). In most cells, GC treatment results in down-regulation of GR mRNA and protein levels via negative feedback mechanisms. However, in GC-treated thymocytes, GR protein levels are maintained at a high level, increasing sensitivity of thymocytes to GCs, resulting in apoptosis termed glucocorticoid-induced cell death (GICD). CD4(+)CD8(+) double-positive thymocytes and thymic natural killer T cells in particular are highly sensitive to GICD. Although GICD is exploited via the use of synthetic GC analogues in the treatment of hematopoietic malignancies, the intracellular molecular pathway of GICD is not well understood. To explore GICD in thymocytes, the authors performed whole genome expression microarray analysis in mouse GR exon 2 null vs wild-type thymus RNA 3 hours after dexamethasone treatment. Identified and validated direct GR targets included P21 and Bim, in addition to an important transcriptional regulator Nfil3, which previously has been associated with GICD and is essential for natural killer cell development in vivo. Immunostaining of NFIL3 in whole thymus localized NFIL3 primarily to the medullary region, and double labeling colocalized NFIL3 to apoptotic cells. In silico analysis revealed a putative GC response element 5 kb upstream of the Nfil3 promoter that is strongly conserved in the rat genome and was confirmed to bind GR by chromatin immunoprecipitation. The knockdown of Nfil3 mRNA levels to 20% of normal using specific small interfering RNAs abrogated GICD, indicating that NFIL3 is required for normal GICD in CTLL-2 T cells.</abstract>
<description>Published Version</description>
<description>Copyright © 2013 by The Endocrine Society</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC)</description>
<dateAccepted>2014-06-16T15:51:42Z</dateAccepted>
<available>2014-06-16T15:51:42Z</available>
<created>2014-06-16T15:51:42Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Endocrine Society</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1020770</relation>
<isPartOf type="series">Endocrinology</isPartOf>
<bibliographicCitation type="volume">54</bibliographicCitation>
<bibliographicCitation type="issue">4</bibliographicCitation>
<bibliographicCitation type="issn">0013-7227</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39663</identifier>
<subject>animals</subject><subject>apoptosis/physiology</subject><subject>basic-leucine zipper transcription factors/metabolism</subject><subject>basic-leucine zipper transcription factors/physiology</subject><subject>cells</subject><subject>cultured</subject><subject>gene expression regulation</subject><subject>gene knockdown techniques</subject><subject>glucocorticoids/physiology</subject><subject>male</subject><subject>mice</subject><subject>receptors</subject><subject>glucocorticoid/physiology</subject><subject>thymocytes/metabolism</subject><subject>thymocytes/physiology</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version></work><work id="179621398" url="/work/179621398"><troveUrl>http://trove.nla.gov.au/work/179621398</troveUrl><title>Human and mouse type I natural killer T cell antigen receptors exhibit different fine specificities for CD1d-antigen complex</title><contributor>Wun, Kwok</contributor><contributor> Ross, Fiona</contributor><contributor> Patel, Onisha</contributor><contributor> Besra, Gurdyal</contributor><contributor> Porcelli, Steven</contributor><contributor> Richardson, Stewart</contributor><contributor> Keshipeddy, Santosh</contributor><contributor> Howell, Amy</contributor><contributor> Godfrey, Dale</contributor><contributor> Rossjohn, Jamie</contributor><issued>2012</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>) Published Version © 2012 by The American Society</snippet><identifier type="url" linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/836816</identifier><version id="211037985"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/44145</identifier><datestamp>2017-08-28T14:37:07Z</datestamp><setSpec>com_11343_225</setSpec><setSpec>com_11343_164</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_226</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>Human and Mouse Type I Natural Killer T Cell Antigen Receptors Exhibit Different Fine Specificities for CD1d-Antigen Complex</title>
<creator>Wun, KS</creator>
<creator>Ross, F</creator>
<creator>Patel, O</creator>
<creator>Besra, GS</creator>
<creator>Porcelli, SA</creator>
<creator>Richardson, SK</creator>
<creator>Keshipeddy, S</creator>
<creator>Howell, AR</creator>
<creator>Godfrey, DI</creator>
<creator>Rossjohn, J</creator>
























<abstract>Human and mouse type I natural killer T (NKT) cells respond to a variety of CD1d-restricted glycolipid antigens (Ags), with their NKT cell antigen receptors (NKT TCRs) exhibiting reciprocal cross-species reactivity that is underpinned by a conserved NKT TCR-CD1d-Ag docking mode. Within this common docking footprint, the NKT TCR recognizes, to varying degrees of affinity, a range of Ags. Presently, it is unclear whether the human NKT TCRs will mirror the generalities underpinning the fine specificity of the mouse NKT TCR-CD1d-Ag interaction. Here, we assessed human NKT TCR recognition against altered glycolipid ligands of α-galactosylceramide (α-GalCer) and have determined the structures of a human NKT TCR in complex with CD1d-4',4″-deoxy-α-GalCer and CD1d-α-GalCer with a shorter, di-unsaturated acyl chain (C20:2). Altered glycolipid ligands with acyl chain modifications did not affect the affinity of the human NKT TCR-CD1d-Ag interaction. Surprisingly, human NKT TCR recognition is more tolerant to modifications at the 4'-OH position in comparison with the 3'-OH position of α-GalCer, which contrasts the fine specificity of the mouse NKT TCR-CD1d-Ag recognition (4'-OH > 3'-OH). The fine specificity differences between human and mouse NKT TCRs was attributable to differing interactions between the respective complementarity-determining region 1α loops and the Ag. Accordingly, germline encoded fine-specificity differences underpin human and mouse type I NKT TCR interactions, which is an important consideration for therapeutic development and NKT cell physiology.</abstract>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC)</description>
<description>Published Version</description>
<description>© 2012 by The American Society for Biochemistry and Molecular Biology, Inc.</description>
<dateAccepted>2015-01-08T23:18:22Z</dateAccepted>
<available>2015-01-08T23:18:22Z</available>
<created>2015-01-08T23:18:22Z</created>
<issued>2012-11-09</issued>
<type>journal article</type>
<publisher>AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://orcid.org/0000-0002-3009-5472</relation>

<relation>
                    http://doi.org/10.1074/jbc.M112.412320</relation>
<isPartOf type="series">JOURNAL OF BIOLOGICAL CHEMISTRY</isPartOf>
<bibliographicCitation type="volume">287</bibliographicCitation>
<bibliographicCitation type="issue">46</bibliographicCitation>
<bibliographicCitation type="issn">0021-9258</bibliographicCitation>
<bibliographicCitation type="yearIssued">2012-11-09</bibliographicCitation>
<identifier type="dcterms:URI" linktype="fulltext">http://hdl.handle.net/11343/44145</identifier>
<subject>amino acid motifs</subject><subject>animals</subject><subject>antigen presentation</subject><subject>antigens/chemistry</subject><subject>antigens</subject><subject>CD1d/metabolism</subject><subject>crystallography</subject><subject>X-Ray/methods</subject><subject>flow cytometry/methods</subject><subject>glycolipids/chemistry</subject><subject>humans</subject><subject>leukocytes</subject><subject>mononuclear/cytology</subject><subject>lipids/chemistry</subject><subject>mice</subject><subject>models</subject><subject>molecular</subject><subject>molecular conformation</subject><subject>natural killer T-cells/immunology</subject><subject>natural killer T-cells/metabolism</subject><subject>receptors</subject><subject>antigen/metabolism</subject><subject>structure-activity relationship</subject><subject>surface plasmon resonance</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2012-11-09</issued><holdingsCount>1</holdingsCount></version><version id="195498517"><record><header>
        <identifier>monash:116408</identifier>
        <datestamp>2015-01-22T05:43:38.933Z</datestamp>
        <setSpec>active</setSpec>
        <setSpec>VMOU</setSpec>
      </header><metadata>
      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>Human and mouse type I natural killer T cell antigen receptors exhibit different fine specificities for CD1d-antigen complex</title><creator>Wun, Kwok</creator><creator>Ross, Fiona</creator><creator>Patel, Onisha</creator><creator>Besra, Gurdyal</creator><creator>Porcelli, Steven</creator><creator>Richardson, Stewart</creator><creator>Keshipeddy, Santosh</creator><creator>Howell, Amy</creator><creator>Godfrey, Dale</creator><creator>Rossjohn, Jamie</creator><subject>Chemical sciences (03)</subject><subject>Biological sciences (06)</subject><subject>Medical and health sciences (11)</subject><publisher>American Society for Biochemistry and Molecular Biology Inc.</publisher><date>2012</date><type>text</type><type>journal article</type><identifier linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/836816</identifier><identifier>monash:116408</identifier><language>eng</language><relation>Journal Of Biological Chemistry [P], vol. 287, no. 46, p. 39139-39148</relation><relation>urn:ISSN:00219258</relation><rights>Subscription access to fulltext</rights></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2012</issued><holdingsCount>1</holdingsCount></version></work><work id="184623567" url="/work/184623567"><troveUrl>http://trove.nla.gov.au/work/184623567</troveUrl><title>CD73 promotes anthracycline resistance and poor prognosis in triple negative breast cancer</title><contributor>Loi, Sherene</contributor><contributor> Pommey, Sandra</contributor><contributor> Haibe-Kains, Benjamin</contributor><contributor> Beavis, Paul A</contributor><contributor> Darcy, Phillip K</contributor><contributor> Smyth, Mark J</contributor><contributor> Stagg, John</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><type>Article/Report</type><isPartOf url="/work/3423224">Proceedings of the National Academy of Sciences of the United
States</isPartOf><holdingsCount>2</holdingsCount><versionCount>3</versionCount><relevance score="0.0098551065">limited relevance</relevance><snippet> in TNBC.

  ectonucleotidase | immunogenic cell death | immunotherapy

  www.pnas.<b>org</b>/cgi/doi/ 10.1073/pnas.1222251110

 Loi</snippet><identifier type="url" linktype="restricted">http://dx.doi.org/10.1073/pnas.1222251110</identifier><version id="204001492"><record><identifier type="galeAccessionNumber">349901785</identifier><bibliographicCitation type="yearIssued">2013</bibliographicCitation><bibliographicCitation type="dateIssued">July 2</bibliographicCitation><bibliographicCitation type="volume">110</bibliographicCitation><bibliographicCitation type="issue">27</bibliographicCitation><issued type="dcterms:W3CDTF">2013-07-02</issued><title>CD73 promotes anthracycline resistance and poor prognosis in
triple negative breast cancer.(IMMUNOLOGY)(Report)(Author
abstract)</title><language>English</language><alternative>CD73 promotes anthracycline resistance and poor
prognosis in triple negative breast cancer.</alternative><creator>Loi, Sherene</creator><creator>Pommey, Sandra</creator><creator>Haibe-Kains, Benjamin</creator><creator>Beavis, Paul A.</creator><creator>Darcy, Phillip K.</creator><creator>Smyth, Mark J.</creator><creator>Stagg, John</creator><description type="byline">Loi, Sherene^Pommey, Sandra^Haibe-Kains, Benjamin^Beavis, Paul
A.^ Darcy, Phillip K.^Smyth, Mark J.^Stagg, John</description><bibliographicCitation type="pagination">11091(6)</bibliographicCitation><subject code="8000421" type="productCode">Cancer Diagnosis</subject><subject code="6215" type="NAICS">Medical and Diagnostic Laboratories</subject><subject>Anthracyclines -- Dosage and administration</subject><subject>Breast cancer -- Physiological aspects</subject><subject>Breast cancer -- Prognosis</subject><subject>Cancer -- Diagnosis</subject><subject>Cancer -- Research</subject><type>Author abstract</type><type>Report</type><subject>Anthracyclines -- Dosage and administration</subject><subject>Breast cancer -- Physiological aspects</subject><subject>Breast cancer -- Prognosis</subject><subject>Cancer diagnosis -- Research</subject><subject code="310" type="eventCode">Science & research</subject><subject type="topicalScope">Dosage and administration</subject><subject type="topicalScope">Physiological aspects</subject><subject type="topicalScope">Prognosis</subject><subject type="topicalScope">Research</subject><isPartOf code="GALE2749" type="publication">Proceedings of the National Academy of Sciences of the United
States</isPartOf><publisher>National Academy of Sciences</publisher><audience>Academic</audience><medium type="publication">Magazine/Journal article</medium><subject>Science and technology</subject><rights type="publisher">COPYRIGHT 2013 National Academy of
Sciences</rights><bibliographicCitation type="issn">0027-8424</bibliographicCitation><rights type="metadata">Copyright 2013 Gale, Cengage Learning.  All rights
reserved.</rights><abstract type="author">
  Using gene-expression data from over 6,000 breast cancer patients,
we report herein that high CD73 expression is associated with a poor
prognosis in triple-negative breast cancers (TNBC). Because
anthracycline-based chemotherapy regimens are standard treatment for
TNBC, we investigated the relationship between CD73 and anthracycline
efficacy. In TNBC patients treated with anthracycline-only preoperative
chemotherapy, high CD73 gene expression was significantly associated
with a lower rate of pathological complete response or the disappearance
of invasive tumor at surgery. Using mouse models of breast cancer, we
demonstrated that CD73 overexpression in tumor cells conferred
chemoresistance to doxorubicin, a commonly used anthracycline, by
suppressing adaptive antitumor immune responses via activation of A2A
adenosine receptors. Targeted blockade of CD73 enhanced
doxorubicin-mediated antitumor immune responses and significantly
prolonged the survival of mice with established metastatic breast
cancer. Taken together, our data suggest that CD73 constitutes a
therapeutic target in TNBC.

  ectonucleotidase | immunogenic cell death | immunotherapy

  www.pnas.org/cgi/doi/ 10.1073/pnas.1222251110

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<title>CD73 promotes anthracycline resistance and poor prognosis in triple negative breast cancer</title>
<creator>Loi, S</creator>
<creator>Pommey, S</creator>
<creator>Haibe-Kains, B</creator>
<creator>Beavis, PA</creator>
<creator>Darcy, PK</creator>
<creator>Smyth, MJ</creator>
<creator>Stagg, J</creator>
<contributor>Loi, Sherene [0000-0001-6137-9171]</contributor>
<contributor>Haibe-Kains, Benjamin [0000-0002-7684-0079]</contributor>
<contributor>Smyth, Mark J [0000-0001-7098-7240]</contributor>



<abstract>Using gene-expression data from over 6,000 breast cancer patients, we report herein that high CD73 expression is associated with a poor prognosis in triple-negative breast cancers (TNBC). Because anthracycline-based chemotherapy regimens are standard treatment for TNBC, we investigated the relationship between CD73 and anthracycline efficacy. In TNBC patients treated with anthracycline-only preoperative chemotherapy, high CD73 gene expression was significantly associated with a lower rate of pathological complete response or the disappearance of invasive tumor at surgery. Using mouse models of breast cancer, we demonstrated that CD73 overexpression in tumor cells conferred chemoresistance to doxorubicin, a commonly used anthracycline, by suppressing adaptive antitumor immune responses via activation of A2A adenosine receptors. Targeted blockade of CD73 enhanced doxorubicin-mediated antitumor immune responses and significantly prolonged the survival of mice with established metastatic breast cancer. Taken together, our data suggest that CD73 constitutes a therapeutic target in TNBC.</abstract>
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<created>2014-08-19T01:29:09Z</created>
<issued>2013-07-02</issued>
<type>journal article</type>
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<subject>ectonucleotidase</subject><subject>immunogenic cell death</subject><subject>immunotherapy</subject></qualifieddc>
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        <bibliographicCitation>
        Loi, Sherene, Pommey, Sandra, Haibe-Kains, Benjamin, Beavis, Paul A., Darcy, Phillip K., Smyth, Mark J. and Stagg, John (2013) CD73 promotes anthracycline resistance and poor prognosis in triple negative breast cancer. Proceedings of the National Academy of Sciences of the United States of America, 110 27: 11091-11096. doi:10.1073/pnas.1222251110
    </bibliographicCitation><relation>http://doi.org/10.1073/pnas.1222251110
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			<description>
					Using gene-expression data from over 6,000 breast cancer patients, wereport herein that high CD73 expression is associated with a poor prognosis in triple-negative breast cancers (TNBC). Because anthracycline-based chemotherapy regimens are standard treatment for TNBC, we investigated the relationship between CD73 and anthracycline efficacy. In TNBC patients treated with anthracycline-only preoperative chemotherapy, high CD73 gene expression was significantly associated with a lower rate of pathological complete response or the disappearance of invasive tumor at surgery. Using mouse models of breast cancer, we demonstrated that CD73 overexpression in tumor cells conferred chemoresistance to doxorubicin, a commonly used anthracycline, by suppressing adaptive antitumor immune responses via activation of A2A adenosine receptors. Targeted blockade of CD73 enhanced doxorubicin-mediated antitumor immune responses and significantly prolonged the survival of mice with established metastatic breast cancer. Taken together, our data suggest that CD73 constitutes a therapeutic target in TNBC.
				</description>
	
        <type>journal article</type>
        <date>2013-07-01</date>
																        <creator>Loi, Sherene</creator>
							        <creator>Pommey, Sandra</creator>
							        <creator>Haibe-Kains, Benjamin</creator>
							        <creator>Beavis, Paul A.</creator>
							        <creator>Darcy, Phillip K.</creator>
							        <creator>Smyth, Mark J.</creator>
							        <creator>Stagg, John</creator>
											
																        <subject>Ectonucleotidase</subject>
							        <subject>Immunogenic cell death</subject>
							        <subject>Immunotherapy</subject>
									        
		

		
		

						        	<publisher>National Academy of Sciences</publisher>
												        			      			      <language>eng</language>
			      					

		


		        <identifier linktype="notonline">http://espace.library.uq.edu.au/view/UQ:308636</identifier>

		
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of lenalidomide therapy</title><contributor>Chan, A. C</contributor><contributor> Neeson, P</contributor><contributor> Leeansyah, E</contributor><contributor> Tainton, K</contributor><contributor> Quach, H</contributor><contributor> Prince, H. M</contributor><contributor> Harrison, S. J</contributor><contributor> Godfrey, D. I</contributor><contributor> Ritchie, D</contributor><contributor> Berzins, S. P</contributor><issued>2014</issued><type>Article</type><type>Article/Journal or magazine article</type><isPartOf url="/work/11248735">Clinical and Experimental Immunology</isPartOf><holdingsCount>1</holdingsCount><versionCount>2</versionCount><relevance score="0.008623218">limited relevance</relevance><snippet> funded in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b>). Fulltext</snippet><version id="211626169"><record><header>
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<title>Natural killer T cell defects in multiple myeloma and the impact of lenalidomide therapy</title>
<creator>Chan, A. C.</creator>
<creator>Neeson, P.</creator>
<creator>Leeansyah, E.</creator>
<creator>Tainton, K.</creator>
<creator>Quach, H.</creator>
<creator>Prince, H. M.</creator>
<creator>Harrison, S. J.</creator>
<creator>Godfrey, D. I.</creator>
<creator>Ritchie, D.</creator>
<creator>Berzins, S. P.</creator>










<abstract>The causes of multiple myeloma (MM) remain obscure and there are few known risk factors; however, natural killer T (NKT) cell abnormalities have been reported in patients with MM, and therapeutic targeting of NKT cells is promoted as a potential treatment. We characterized NKT cell defects in treated and untreated patients with MM and determined the impact of lenalidomide therapy on the NKT cell pool. Lenalidomide is an immunomodulatory drug with co-stimulatory effects on NKT cells in vitro and is an approved treatment for MM, although its mode of action in that context is not well defined. We find that patients with relapsed/progressive MM had a marked deficiency in NKT cell numbers. In contrast, newly diagnosed patients had relatively normal NKT cell frequency and function prior to treatment, although a specific NKT cell deficiency emerged after high-dose melphalan and autologous stem cell transplantation (ASCT) regimen. This also impacted NK cells and conventional T cells, but the recovery of NKT cells was considerably delayed, resulting in a prolonged, treatment-induced NKT cell deficit. Longitudinal analysis of individual patients revealed that lenalidomide therapy had no in-vivo impact on NKT cell numbers or cytokine production, either as induction therapy, or as maintenance therapy following ASCT, indicating that its clinical benefits in this setting are independent of NKT cell modulation.</abstract>
<description>Published Version</description>
<description>© 2013 British Society for Immunology</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<description>Fulltext embargoed for: 12 months post date of publication</description>
<dateAccepted>2014-06-16T15:54:39Z</dateAccepted>
<available>2014-06-16T15:54:39Z</available>
<created>2014-06-16T15:54:39Z</created>
<issued>2014</issued>
<type>journal article</type>
<publisher>Wiley-Blackwell</publisher>
<relation>
                http://purl.org/au-research/grants/NHMRC/1013667</relation>
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                http://purl.org/au-research/grants/NHMRC/1020770</relation>
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                http://purl.org/au-research/grants/NHMRC/454363</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/251608</relation>
<relation>
                http://purl.org/au-research/grants/NHMRC/454569</relation>
<relation>
					http://doi.org/10.1111/cei.12196</relation>
<isPartOf type="series">Clinical and Experimental Immunology</isPartOf>
<bibliographicCitation type="volume">175</bibliographicCitation>
<bibliographicCitation type="issue">1</bibliographicCitation>
<bibliographicCitation type="yearIssued">2014</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39707</identifier>
<subject>NKT cells</subject><subject>tumor-immunity</subject><subject>myelodysplastic syndrome</subject><subject>antitumor immunity</subject><subject>activation</subject><subject>subsets</subject><subject>cancer</subject><subject>progression</subject><subject>disease</subject><subject>CD1d</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2014</issued><holdingsCount>1</holdingsCount></version><version id="204494632"><record><identifier type="galeAccessionNumber">351350041</identifier><bibliographicCitation type="yearIssued">2014</bibliographicCitation><bibliographicCitation type="dateIssued">Jan</bibliographicCitation><bibliographicCitation type="volume">175</bibliographicCitation><bibliographicCitation type="issue">1</bibliographicCitation><issued type="dcterms:W3CDTF">2014-01-01</issued><title>Natural killer T cell defects in multiple myeloma and the impact
of lenalidomide therapy.</title><language>English</language><creator>Chan, A. C.</creator><creator>Neeson, P.</creator><creator>Leeansyah, E.</creator><creator>Tainton, K.</creator><creator>Quach, H.</creator><creator>Prince, H. M.</creator><creator>Harrison, S. J.</creator><creator>Godfrey, D. I.</creator><creator>Ritchie, D.</creator><creator>Berzins, S. P.</creator><description type="byline">A. C. Chan, P. Neeson, E. Leeansyah, K. Tainton, H. Quach, H. M.
Prince, S. J. Harrison, D. I. Godfrey, D. Ritchie, S. P.
Berzins</description><bibliographicCitation type="pagination">49(10)</bibliographicCitation><subject>Multiple myeloma -- Development and progression</subject><subject>Multiple myeloma -- Analysis</subject><subject>T cells -- Analysis</subject><subject>Stem cells -- Analysis</subject><subject>Drug approval -- Analysis</subject><subject>Angiogenesis inhibitors -- Analysis</subject><subject>Multiple myeloma -- Development and progression</subject><subject>Multiple myeloma -- Analysis</subject><subject>T cells -- Analysis</subject><subject>Stem cells -- Analysis</subject><subject>Drug approval -- Analysis</subject><subject>Lenalidomide -- Analysis</subject><subject>Angiogenesis inhibitors -- Analysis</subject><subject type="topicalScope">Analysis</subject><subject type="topicalScope">Development and progression</subject><isPartOf code="GALE5JDV" type="publication">Clinical and Experimental Immunology</isPartOf><publisher>Wiley Subscription Services, Inc.</publisher><audience>Academic</audience><medium type="publication">Magazine/Journal article</medium><subject>Health</subject><rights type="publisher">COPYRIGHT 2014 Blackwell Publishers
Ltd.</rights><bibliographicCitation type="issn">0009-9104</bibliographicCitation><rights type="metadata">Copyright 2014 Gale, Cengage Learning.  All rights
reserved.</rights><abstract type="author">
  Byline: A. C. Chan, P. Neeson, E. Leeansyah, K. Tainton, H. Quach,
H. M. Prince, S. J. Harrison, D. I. Godfrey, D. Ritchie, S. P. Berzins

  Keywords:

  lenalidomide; multiple myeloma; NKT cells

  Summary

  The causes of multiple myeloma (MM) remain obscure and there are
few known risk factors; however, natural killer T (NKT) cell
abnormalities have been reported in patients with MM, and therapeutic
targeting of NKT cells is promoted as a potential treatment. We
characterized NKT cell defects in treated and untreated patients with MM
and determined the impact of lenalidomide therapy on the NKT cell pool.
Lenalidomide is an immunomodulatory drug with co-stimulatory effects on
NKT cells in vitro and is an approved treatment for MM, although its
mode of action in that context is not well defined. We find that
patients with relapsed/progressive MM had a marked deficiency in NKT
cell numbers. In contrast, newly diagnosed patients had relatively
normal NKT cell frequency and function prior to treatment, although a
specific NKT cell deficiency emerged after high-dose melphalan and
autologous stem cell transplantation (ASCT) regimen. This also impacted
NK cells and conventional T cells, but the recovery of NKT cells was
considerably delayed, resulting in a prolonged, treatment-induced NKT
cell deficit. Longitudinal analysis of individual patients revealed that
lenalidomide therapy had no in-vivo impact on NKT cell numbers or
cytokine production, either as induction therapy, or as maintenance
therapy following ASCT, indicating that its clinical benefits in this
setting are independent of NKT cell modulation.

  Supporting information:

  Additional Supporting Information may be found in the online
version of this article

  CAPTION(S):

  Fig.S1. Multiple myeloma clinical trial design. Previously
untreated newly diagnosed patients were enrolled onto the Litvacc study
(a), where following lenalidomide + dexamethasone (LEN+DEX) induction
the patients received an autologous stem cell transplantation (ASCT)
followed by myeloma lysate-pulsed dendritic cells (DCs)+LEN maintenance
or len maintenance alone (in our study, 10 of 11 patients received
myeloma lysate-pulsed DCs+LEN maintenance). Patients with refractory
relapsed disease were enrolled into the RevLite study (b) to receive
LEN+DEX induction, then repeated cycles of LEN+DEX until disease
progression. A comparison between the two trials is provided in table
(c) including disease state, drug dose and cycles of therapy.

</abstract><metadataSource>GALE</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2014-01-01</issued><holdingsCount>0</holdingsCount></version></work><work id="184274266" url="/work/184274266"><troveUrl>http://trove.nla.gov.au/work/184274266</troveUrl><title>ZBTB7B (Th-POK) regulates the development of IL-17 -producing-CD1d-restricted mouse NKT cells</title><contributor>Enders, Anselm</contributor><contributor> Stankovic, Sanda</contributor><contributor> Teh, Charis</contributor><contributor> Uldrich, Adam P</contributor><contributor> Yabas, Mehmet</contributor><contributor> Juelich, Torsten</contributor><contributor> Altin, John A</contributor><contributor> Frankenreiter, Sandra</contributor><contributor> Bergmann, Hannes</contributor><contributor> Roots, Carla M</contributor><contributor> Kyparissoudis, Konstantinos</contributor><contributor> Goodnow, Chris C</contributor><contributor> Godfrey, Dale I</contributor><issued>2012-2015</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.008623218">limited relevance</relevance><snippet> genetically predetermining the balance of effector subsets within the NKT cell population. <b>NHMRC</b> (National</snippet><identifier type="url" linktype="unknown">http://hdl.handle.net/1885/10400</identifier><version id="200688909 244994152"><record><header><identifier>oai:openresearch-repository.anu.edu.au:1885/10400</identifier><datestamp>2017-04-06T04:10:55Z</datestamp><setSpec>com_1885_9051</setSpec><setSpec>com_1885_1</setSpec><setSpec>col_1885_26</setSpec></header><metadata><dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
<title>ZBTB7B (Th-POK) regulates the development of IL-17 -producing-CD1d-restricted mouse NKT cells</title>
<creator>Enders, Anselm</creator>
<creator>Stankovic, Sanda</creator>
<creator>Teh, Charis</creator>
<creator>Uldrich, Adam P</creator>
<creator>Yabas, Mehmet</creator>
<creator>Juelich, Torsten</creator>
<creator>Altin, John A.</creator>
<creator>Frankenreiter, Sandra</creator>
<creator>Bergmann, Hannes</creator>
<creator>Roots, Carla M.</creator>
<creator>Kyparissoudis, Konstantinos</creator>
<creator>Goodnow, Chris C.</creator>
<creator>Godfrey, Dale I.</creator>
<subject>NKT cells</subject>
<subject>Th-POK</subject>
<subject>ThPOK</subject>
<subject>Zbtb7b</subject>
<subject>IL-17</subject>
<description>CD1d-dependent NKT cells represent a heterogeneous family of effector T cells including CD4+CD8- and CD4-CD8- subsets that respond to glycolipid Ags with rapid and potent cytokine production. NKT cell development is regulated by a unique combination of factors, however very little is known about factors that control the development of NKT subsets. In this study, we analyze a novel mouse strain (helpless) with a mis-sense mutation in the BTB-POZ domain of ZBTB7B and demonstrate that this mutation has dramatic, intrinsic effects on development of NKT cell subsets. Although NKT cell numbers are similar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express CD8. Moreover, the majority of ZBTB7B mutant NKT cells in the thymus are retinoic acid-related orphan receptor γt positive, and a high frequency produce IL-17 while very few produce IFN-γ  or other cytokines, sharply contrasting the profile of normal NKT cells. Mice heterozygous for the helpless mutation also have reduced numbers of CD4+ NKT cells and increased production of IL-17 without an increase in CD8+ cells, suggesting that ZBTB7B acts at multiple stages of NKT cell development. These results reveal ZBTB7B as a critical factor genetically predetermining the balance of effector subsets within the NKT cell population.</description>
<description>NHMRC (National Health and Medical Research Council of Australia)</description>
<date>2013-09-04T02:00:19Z</date>
<date>2013-09-04T02:00:19Z</date>
<date>2012-10-26</date>
<date>2015-12-10T11:31:29Z</date>
<type>journal article</type>
<identifier>0022-1767</identifier>
<identifier>1550-6606</identifier>
<identifier linktype="unknown">http://hdl.handle.net/1885/10400</identifier>
<identifier>10.4049/jimmunol.1201486</identifier>
<relation>http://purl.org/au-research/grants/nhmrc/1009190</relation>
<relation>http://purl.org/au-research/grants/nhmrc/1035858</relation>
<relation>http://purl.org/au-research/grants/nhmrc/1020770</relation>
<relation>http://purl.org/au-research/grants/nhmrc/585490</relation>
<relation>nih ai054523</relation>
<relation>ramaciotti foundation major initiative award 2007</relation>
<rights>http://www.sherpa.ac.uk/romeo/issn/0022-1767/   Author may archive post-print but only on a personal website, not on an Institutional Repository. Pre-print archiving unclear. Author cannot archive publisher's version/PDF but may use, if part of a thesis/dissertation, within a thesis repository. Pre-print archiving may be considered prior publication. Set statement must accompany article (see policy link).  Must link to publisher version - from SHERPA/RoMEO site (as at 3/9/13)</rights>
<format>10 + 5 pages</format>
<publisher>American Association of Immunologists</publisher>
<source>Journal of Immunology 189.11 (2012): 5240-5249</source>
<source>http://www.jimmunol.org/content/189/11/5240</source>
</dc>
</metadata><metadataSource type="nuc">ANU:IR</metadataSource></record><record><header><identifier>oai:digitalcollections.anu.edu.au:1885/10400</identifier><datestamp>2015-12-10T11:31:29Z</datestamp><setSpec>com_1885_9051</setSpec><setSpec>com_1885_1</setSpec><setSpec>col_1885_26</setSpec></header><metadata><dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
<title>ZBTB7B (Th-POK) regulates the development of IL-17 -producing-CD1d-restricted mouse NKT cells</title>
<creator>Enders, Anselm</creator>
<creator>Stankovic, Sanda</creator>
<creator>Teh, Charis</creator>
<creator>Uldrich, Adam P</creator>
<creator>Yabas, Mehmet</creator>
<creator>Juelich, Torsten</creator>
<creator>Altin, John A.</creator>
<creator>Frankenreiter, Sandra</creator>
<creator>Bergmann, Hannes</creator>
<creator>Roots, Carla M.</creator>
<creator>Kyparissoudis, Konstantinos</creator>
<creator>Goodnow, Chris C.</creator>
<creator>Godfrey, Dale I.</creator>
<subject>NKT cells</subject>
<subject>Th-POK</subject>
<subject>ThPOK</subject>
<subject>Zbtb7b</subject>
<subject>IL-17</subject>
<description>CD1d-dependent NKT cells represent a heterogeneous family of effector T cells including CD4+CD8- and CD4-CD8- subsets that respond to glycolipid Ags with rapid and potent cytokine production. NKT cell development is regulated by a unique combination of factors, however very little is known about factors that control the development of NKT subsets. In this study, we analyze a novel mouse strain (helpless) with a mis-sense mutation in the BTB-POZ domain of ZBTB7B and demonstrate that this mutation has dramatic, intrinsic effects on development of NKT cell subsets. Although NKT cell numbers are similar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express CD8. Moreover, the majority of ZBTB7B mutant NKT cells in the thymus are retinoic acid-related orphan receptor γt positive, and a high frequency produce IL-17 while very few produce IFN-γ  or other cytokines, sharply contrasting the profile of normal NKT cells. Mice heterozygous for the helpless mutation also have reduced numbers of CD4+ NKT cells and increased production of IL-17 without an increase in CD8+ cells, suggesting that ZBTB7B acts at multiple stages of NKT cell development. These results reveal ZBTB7B as a critical factor genetically predetermining the balance of effector subsets within the NKT cell population.</description>
<description>NHMRC (National Health and Medical Research Council of Australia)</description>
<date>2013-09-04T02:00:19Z</date>
<date>2013-09-04T02:00:19Z</date>
<date>2012-10-26</date>
<date>2015-12-10T11:31:29Z</date>
<type>journal article</type>
<identifier>0022-1767</identifier>
<identifier>1550-6606</identifier>
<identifier linktype="unknown">http://hdl.handle.net/1885/10400</identifier>
<relation>http://purl.org/au-research/grants/nhmrc/1009190</relation>
<relation>http://purl.org/au-research/grants/nhmrc/1035858</relation>
<relation>http://purl.org/au-research/grants/nhmrc/1020770</relation>
<relation>http://purl.org/au-research/grants/nhmrc/585490</relation>
<relation>nih ai054523</relation>
<relation>ramaciotti foundation major initiative award 2007</relation>
<rights>http://www.sherpa.ac.uk/romeo/issn/0022-1767/   Author may archive post-print but only on a personal website, not on an Institutional Repository. Pre-print archiving unclear. Author cannot archive publisher's version/PDF but may use, if part of a thesis/dissertation, within a thesis repository. Pre-print archiving may be considered prior publication. Set statement must accompany article (see policy link).  Must link to publisher version - from SHERPA/RoMEO site (as at 3/9/13)</rights>
<format>10 + 5 pages</format>
<publisher>American Association of Immunologists</publisher>
<source>Journal of Immunology 189.11 (2012): 5240-5249</source>
<source>http://www.jimmunol.org/content/189/11/5240</source>
</dc>
</metadata><metadataSource type="nuc">ANU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><issued>2012</issued><issued>2015</issued><holdingsCount>1</holdingsCount></version><version id="209154748"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/39650</identifier><datestamp>2017-07-28T11:05:57Z</datestamp><setSpec>com_11343_225</setSpec><setSpec>com_11343_164</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_226</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>ZBTB7B (Th-POK) regulates the development of IL-17-producing CD1d-restricted mouse NKT cells</title>
<creator>Enders, Anselm</creator>
<creator>STANKOVIC, SANDA</creator>
<creator>Teh, Charis</creator>
<creator>Uldrich, Adam P.</creator>
<creator>Yabas, Mehmet</creator>
<creator>Juelich, Torsten</creator>
<creator>Altin, John A.</creator>
<creator>Frankenreiter, Sandra</creator>
<creator>Bergmann, Hannes</creator>
<creator>Roots, Carla M.</creator>
<creator>KYPARISSOUDIS, KONSTANTINOS</creator>
<creator>Goodnow, Chris C.</creator>
<creator>GODFREY, DALE I.</creator>










































<abstract>CD1d-dependent NKT cells represent a heterogeneous family of effector T cells including CD4(+)CD8(-) and CD4(-)CD8(-) subsets that respond to glycolipid Ags with rapid and potent cytokine production. NKT cell development is regulated by a unique combination of factors, however very little is known about factors that control the development of NKT subsets. In this study, we analyze a novel mouse strain (helpless) with a mis-sense mutation in the BTB-POZ domain of ZBTB7B and demonstrate that this mutation has dramatic, intrinsic effects on development of NKT cell subsets. Although NKT cell numbers are similar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express CD8. Moreover, the majority of ZBTB7B mutant NKT cells in the thymus are retinoic acid-related orphan receptor γt positive, and a high frequency produce IL-17 while very few produce IFN-γ or other cytokines, sharply contrasting the profile of normal NKT cells. Mice heterozygous for the helpless mutation also have reduced numbers of CD4(+) NKT cells and increased production of IL-17 without an increase in CD8(+) cells, suggesting that ZBTB7B acts at multiple stages of NKT cell development. These results reveal ZBTB7B as a critical factor genetically predetermining the balance of effector subsets within the NKT cell population.</abstract>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC)</description>
<description>Published Version</description>
<description>Copyright © 2012 by The American Association of Immunologists</description>
<dateAccepted>2014-06-16T15:50:53Z</dateAccepted>
<available>2014-06-16T15:50:53Z</available>
<created>2014-06-16T15:50:53Z</created>
<issued>2012</issued>
<type>journal article</type>
<publisher>American Association of Immunologists</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                    http://doi.org/10.4049/jimmunol.1201486</relation>
<isPartOf type="series">Journal of Immunology</isPartOf>
<bibliographicCitation type="volume">189</bibliographicCitation>
<bibliographicCitation type="issue">11</bibliographicCitation>
<bibliographicCitation type="issn">0022-1767</bibliographicCitation>
<bibliographicCitation type="yearIssued">2012</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39650</identifier>
<subject>animals</subject><subject>antigens</subject><subject>CD1d/genetics</subject><subject>antigens</subject><subject>CD1d/immunology</subject><subject>CD4-positive T-lymphocytes/immunology</subject><subject>CD4-positive T-lymphocytes/metabolism</subject><subject>CD4-positive T-lymphocytes/pathology</subject><subject>CD8-positive T-lymphocytes/immunology</subject><subject>CD8-Positive T-lymphocytes/metabolism</subject><subject>CD8-positive T-lymphocytes/pathology</subject><subject>cell differentiation/immunology</subject><subject>cell proliferation</subject><subject>DNA-binding proteins/genetics</subject><subject>DNA-binding proteins/immunology</subject><subject>gene expression/immunology</subject><subject>Interferon-gamma/biosynthesis</subject><subject>Interferon-gamma/immunology</subject><subject>Interleukin-17/biosynthesis</subject><subject>Interleukin-17/immunology</subject><subject>male</subject><subject>mice</subject><subject>mice</subject><subject>transgenic</subject><subject>mutation</subject><subject>Missense</subject><subject>natural killer T-cells/immunology</subject><subject>natural killer T-cells/metabolism</subject><subject>natural killer T-cells/pathology</subject><subject>Nuclear Receptor Subfamily 1</subject><subject>Group F</subject><subject>Member 3/genetics</subject><subject>Member 3/immunology</subject><subject>tertiary protein structure</subject><subject>T-lymphocyte Subsets/immunology</subject><subject>T-lymphocyte Subsets/metabolism</subject><subject>T-lymphocyte Subsets/pathology</subject><subject>thymus gland/immunology</subject><subject>thymus gland/metabolism</subject><subject>thymus gland/pathology</subject><subject>transcription factors/genetics</subject><subject>transcription factors/immunology</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2012</issued><holdingsCount>1</holdingsCount></version></work><work id="191159237" url="/work/191159237"><troveUrl>http://trove.nla.gov.au/work/191159237</troveUrl><title>Recognition of microbial and mammalian phospholipid antigens by NKT cells with diverse TCRs</title><contributor>Tatituri, RVV</contributor><contributor> Watts, GFM</contributor><contributor> Bhowruth, V</contributor><contributor> Barton, N</contributor><contributor> Rothchild, A</contributor><contributor> Hsu, F-F</contributor><contributor> Almeida, CF</contributor><contributor> Cox, LR</contributor><contributor> Eggeling, L</contributor><contributor> Cardell, S</contributor><contributor> Rossjohn, J</contributor><contributor> Godfrey, DI</contributor><contributor> Behar, SM</contributor><contributor> Besra, GS</contributor><contributor> Brenner, MB</contributor><contributor> Brigl, M</contributor><contributor> Cox, Liam R [0000-0001-7018-3904]</contributor><contributor> Rossjohn, Jamie [0000-0002-2020-7522]</contributor><contributor> Behar, Samuel M [0000-0002-3374-6699]</contributor><contributor> Besra, Gurdyal S [0000-0002-5605-0395]</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>2</holdingsCount><versionCount>2</versionCount><relevance score="0.008623218">limited relevance</relevance><snippet> and Medical <b>Research</b> Council (<b>NHMRC</b>) </snippet><identifier type="url" linktype="fulltext">http://arrow.monash.edu.au/hdl/1959.1/933511</identifier><version id="208513280"><record><header>
        <identifier>monash:121113</identifier>
        <datestamp>2015-05-12T05:48:09.891Z</datestamp>
        <setSpec>active</setSpec>
        <setSpec>content</setSpec>
        <setSpec>VMOU</setSpec>
      </header><metadata>
      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>Recognition of microbial and mammalian phospholipid antigens by NKT cells with diverse TCRs</title><creator>Tatituri, Raju</creator><creator>Watts, Gerald</creator><creator>Bhowruth, Veemal</creator><creator>Barton, Nathaniel</creator><creator>Rothchild, Alissa</creator><creator>Hsu, Fong-Fu</creator><creator>Almeida, Catarina</creator><creator>Cox, Liam</creator><creator>Eggeling, Lothar</creator><creator>Cardell, Susanna</creator><creator>Rossjohn, Jamie</creator><creator>Godfrey, Dale</creator><creator>Behar, Samuel</creator><creator>Besra, Gurdyal</creator><creator>Brenner, Michael</creator><creator>Brigl, Manfred</creator><subject>Multidisciplinary (md)</subject><publisher>National Academy of Sciences</publisher><date>2013</date><type>text</type><type>journal article</type><identifier linktype="fulltext">http://arrow.monash.edu.au/hdl/1959.1/933511</identifier><identifier>monash:121113</identifier><language>eng</language><relation>Proceedings Of The National Academy Of Sciences Of The United States Of America [P], vol. 110, no. 5, p. 1827-1832</relation><relation>urn:ISSN:00278424</relation><relation>http://purl.org/au-research/grants/nhmrc/1037233</relation><rights>Open access to fulltext</rights><free_to_read /></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>1</holdingsCount></version><version id="209397312"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/39664</identifier><datestamp>2017-09-25T10:19:23Z</datestamp><setSpec>com_11343_225</setSpec><setSpec>com_11343_164</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_226</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>Recognition of microbial and mammalian phospholipid antigens by NKT cells with diverse TCRs</title>
<creator>Tatituri, RVV</creator>
<creator>Watts, GFM</creator>
<creator>Bhowruth, V</creator>
<creator>Barton, N</creator>
<creator>Rothchild, A</creator>
<creator>Hsu, F-F</creator>
<creator>Almeida, CF</creator>
<creator>Cox, LR</creator>
<creator>Eggeling, L</creator>
<creator>Cardell, S</creator>
<creator>Rossjohn, J</creator>
<creator>Godfrey, DI</creator>
<creator>Behar, SM</creator>
<creator>Besra, GS</creator>
<creator>Brenner, MB</creator>
<creator>Brigl, M</creator>
<contributor>Cox, Liam R [0000-0001-7018-3904]</contributor>
<contributor>Rossjohn, Jamie [0000-0002-2020-7522]</contributor>
<contributor>Behar, Samuel M [0000-0002-3374-6699]</contributor>
<contributor>Besra, Gurdyal S [0000-0002-5605-0395]</contributor>




























































<abstract>CD1d-restricted natural killer T (NKT) cells include two major subgroups. The most widely studied are Vα14Jα18(+) invariant NKT (iNKT) cells that recognize the prototypical α-galactosylceramide antigen, whereas the other major group uses diverse T-cell receptor (TCR) α-and β-chains, does not recognize α-galactosylceramide, and is referred to as diverse NKT (dNKT) cells. dNKT cells play important roles during infection and autoimmunity, but the antigens they recognize remain poorly understood. Here, we identified phosphatidylglycerol (PG), diphosphatidylglycerol (DPG, or cardiolipin), and phosphatidylinositol from Mycobacterium tuberculosis or Corynebacterium glutamicum as microbial antigens that stimulated various dNKT, but not iNKT, hybridomas. dNKT hybridomas showed distinct reactivities for diverse antigens. Stimulation of dNKT hybridomas by microbial PG was independent of Toll-like receptor-mediated signaling by antigen-presenting cells and required lipid uptake and/or processing. Furthermore, microbial PG bound to CD1d molecules and plate-bound PG/CD1d complexes stimulated dNKT hybridomas, indicating direct recognition by the dNKT cell TCR. Interestingly, despite structural differences in acyl chain composition between microbial and mammalian PG and DPG, lipids from both sources stimulated dNKT hybridomas, suggesting that presentation of microbial lipids and enhanced availability of stimulatory self-lipids may both contribute to dNKT cell activation during infection.</abstract>
<description>Published Version</description>
<description>© 2013 The Authors</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC)</description>
<dateAccepted>2014-06-16T15:51:46Z</dateAccepted>
<available>2014-06-16T15:51:46Z</available>
<created>2014-06-16T15:51:46Z</created>
<issued>2013-01-29</issued>
<type>journal article</type>
<publisher>NATL ACAD SCIENCES</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1021972</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1020770</relation>
<relation>
                    http://orcid.org/0000-0001-7018-3904</relation>
<relation>
                    http://orcid.org/0000-0002-2020-7522</relation>
<relation>
                    http://orcid.org/0000-0002-3009-5472</relation>
<relation>
                    http://orcid.org/0000-0002-3374-6699</relation>
<relation>
                    http://orcid.org/0000-0002-5605-0395</relation>
<relation>
                    http://doi.org/10.1073/pnas.1220601110</relation>
<isPartOf type="series">PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA</isPartOf>
<bibliographicCitation type="volume">110</bibliographicCitation>
<bibliographicCitation type="issue">5</bibliographicCitation>
<bibliographicCitation type="issn">0027-8424</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013-01-29</bibliographicCitation>
<identifier type="dcterms:URI" linktype="notonline">http://hdl.handle.net/11343/39664</identifier>
<subject>animals</subject><subject>antigen-presenting cells/immunology</subject><subject>antigen-presenting cells/metabolism</subject><subject>antigens</subject><subject>bacterial/immunology</subject><subject>antigens</subject><subject>bacterial/metabolism</subject><subject>antigens</subject><subject>cd1d/genetics</subject><subject>antigens</subject><subject>cd1d/immunology</subject><subject>antigens</subject><subject>CDcd1d/metabolism</subject><subject>bacterial proteins/genetics</subject><subject>bacterial proteins/immunology</subject><subject>bacterial proteins/metabolism</subject><subject>cardiolipins/immunology</subject><subject>cardiolipins/metabolism</subject><subject>cell line</subject><subject>cells</subject><subject>cultured</subject><subject>corynebacterium glutamicum/genetics</subject><subject>corynebacterium glutamicum/immunology</subject><subject>corynebacterium glutamicum/metabolism</subject><subject>galactosylceramides/immunology</subject><subject>galactosylceramides/metabolism</subject><subject>hybridomas/immunology</subject><subject>hybridomas/metabolism</subject><subject>macrophages/immunology</subject><subject>macrophages/metabolism</subject><subject>macrophages/microbiology</subject><subject>mice</subject><subject>mice</subject><subject>inbred C57BL</subject><subject>mice</subject><subject>knockout</subject><subject>mycobacterium tuberculosis/immunology</subject><subject>mycobacterium tuberculosis/metabolism</subject><subject>myeloid differentiation factor 88/genetics</subject><subject>myeloid differentiation factor 88/immunology</subject><subject>myeloid differentiation factor 88/metabolism</subject><subject>natural killer t-cells/immunology</subject><subject>natural killer t-cells/metabolism</subject><subject>phosphatidylglycerols/immunology</subject><subject>phosphatidylglycerols/metabolism</subject><subject>phospholipids/immunology</subject><subject>phospholipids/metabolism</subject><subject>receptors</subject><subject>antigen</subject><subject>t-cell</subject><subject>alpha-beta/immunology</subject><subject>receptors</subject><subject>antigen</subject><subject>T-cell</subject><subject>alpha-beta/metabolism</subject><subject>toll-like receptors/immunology</subject><subject>toll-like receptors/metabolism</subject><subject>transferases (other substituted phosphate groups)/genetics</subject><subject>transferases (other substituted phosphate groups)/immunology</subject><subject>transferases (other substituted phosphate groups)/metabolism</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013-01-29</issued><holdingsCount>1</holdingsCount></version></work><work id="189906537" url="/work/189906537"><troveUrl>http://trove.nla.gov.au/work/189906537</troveUrl><title>Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells</title><contributor>Reantragoon, Rangsima</contributor><contributor> Corbett, Alexandra</contributor><contributor> Sakala, Isaac</contributor><contributor> Gherardin, Nicholas</contributor><contributor> Furness, John</contributor><contributor> Chen, Zhenjun</contributor><contributor> Eckle, Sidonia</contributor><contributor> Uldrich, Adam</contributor><contributor> Birkinshaw, Richard</contributor><contributor> Patel, Onisha</contributor><contributor> Kostenko, Lyudmila</contributor><contributor> Meehan, Bronwyn</contributor><contributor> Kedzierska, Katherine</contributor><contributor> Liu, Ligong</contributor><contributor> Fairlie, David</contributor><contributor> Hansen, Ted</contributor><contributor> Godfrey, Dale</contributor><contributor> Rossjohn, Jamie</contributor><contributor> McCluskey, James</contributor><contributor> Kjer-Nielsen, Lars</contributor><issued>2013</issued><type>Article</type><type>Article/Journal or magazine article</type><holdingsCount>3</holdingsCount><versionCount>2</versionCount><relevance score="0.008623218">limited relevance</relevance><snippet> in this collection have been funded in whole or in part by the National Health and Medical <b>Research</b> Council (<b>NHMRC</b></snippet><identifier type="url" linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/955583</identifier><version id="208548000 209154764"><record><header><identifier>oai:minerva-access.unimelb.edu.au:11343/39666</identifier><datestamp>2017-07-28T12:18:43Z</datestamp><setSpec>com_11343_225</setSpec><setSpec>com_11343_164</setSpec><setSpec>com_11343_163</setSpec><setSpec>com_11343_159</setSpec><setSpec>col_11343_226</setSpec></header><metadata><qualifieddc schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd">
<title>Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells</title>
<creator>Reantragoon, Rangsima</creator>
<creator>Corbett, Alexandra J.</creator>
<creator>Sakala, Isaac G.</creator>
<creator>Gherardin, Nicholas A.</creator>
<creator>Furness, John B.</creator>
<creator>CHEN, ZHENJUN</creator>
<creator>Eckle, Sidonia B.G.</creator>
<creator>Uldrich, Adam P.</creator>
<creator>Birkinshaw, Richard W.</creator>
<creator>Patel, Onisha</creator>
<creator>KOSTENKO, LYUDMILA</creator>
<creator>MEEHAN, BRONWYN</creator>
<creator>KEDZIERSKA, KATHERINE</creator>
<creator>Liu, Ligong</creator>
<creator>Fairlie, David P.</creator>
<creator>Hansen, Ted H.</creator>
<creator>GODFREY, DALE I.</creator>
<creator>ROSSJOHN, JAMIE</creator>
<creator>MCCLUSKEY, JAMES</creator>
<creator>KJER-NIELSEN, LARS</creator>










<abstract>Mucosal-associated invariant T cells (MAIT cells) express a semi-invariant T cell receptor (TCR) alpha-chain, TRAV1-2-TRAJ33, and are activated by vitamin B metabolites bound by the major histocompatibility complex (MHC)-related class I-like molecule, MR1. Understanding MAIT cell biology has been restrained by the lack of reagents to specifically identify and characterize these cells. Furthermore, the use of surrogate markers may misrepresent the MAIT cell population. We show that modified human MR1 tetramers loaded with the potent MAIT cell ligand, reduced 6-hydroxymethyl-8-D-ribityllumazine (rRL-6-CH2OH), specifically detect all human MAIT cells. Tetramer(+) MAIT subsets were predominantly CD8(+) or CD4(-)CD8(-), although a small subset of CD4(+) MAIT cells was also detected. Notably, most human CD8(+) MAIT cells were CD8 alpha(+)CD8 beta(-/lo), implying predominant expression of CD8 alpha alpha homodimers. Tetramer-sorted MAIT cells displayed a T(H)1 cytokine phenotype upon antigen-specific activation. Similarly, mouse MR1-rRL-6-CH2OH tetramers detected CD4(+), CD4(-)CD8(-) and CD8(+) MAIT cells in V. 19 transgenic mice. Both human and mouse MAIT cells expressed a broad TCR-beta repertoire, and although the majority of human MAIT cells expressed TRAV1-2-TRAJ33, some expressed TRAJ12 or TRAJ20 genes in conjunction with TRAV1-2. Accordingly, MR1 tetramers allow precise phenotypic characterization of human and mouse MAIT cells and revealed unanticipated TCR heterogeneity in this population.</abstract>
<description>Published Version</description>
<description>© 2013 Reantragoon et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial– Share Alike 3.0 Unported license, as described at http://creativecommons .org/licenses/by-nc-sa/3.0/).</description>
<description>The research outputs in this collection have been funded in whole or in part by the National Health and Medical Research Council (NHMRC).</description>
<dateAccepted>2014-06-16T15:51:56Z</dateAccepted>
<available>2014-06-16T15:51:56Z</available>
<created>2014-06-16T15:51:56Z</created>
<issued>2013</issued>
<type>journal article</type>
<publisher>Rockefeller University Press</publisher>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1013667</relation>
<relation>
                    http://purl.org/au-research/grants/NHMRC/1020770</relation>
<isPartOf type="series">Journal of Experimental Medicine</isPartOf>
<bibliographicCitation type="volume">210</bibliographicCitation>
<bibliographicCitation type="issue">11</bibliographicCitation>
<bibliographicCitation type="issn">0022-1007</bibliographicCitation>
<bibliographicCitation type="yearIssued">2013</bibliographicCitation>
<identifier type="dcterms:URI" linktype="fulltext">http://hdl.handle.net/11343/39666</identifier>
<subject>vitamin-b metabolites</subject><subject>mait cells</subject><subject>alpha-chain</subject><subject>bacterial-infection</subject><subject>CD1d tetramers</subject><subject>recognition</subject><subject>lymphocytes</subject><subject>repertoire</subject><subject>selection</subject><subject>peptide</subject></qualifieddc>
</metadata><metadataSource type="nuc">VU:IR</metadataSource></record><record><header>
        <identifier>monash:126899</identifier>
        <datestamp>2015-02-03T02:51:54.113Z</datestamp>
        <setSpec>active</setSpec>
        <setSpec>VMOU</setSpec>
      </header><metadata>
      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><title>Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells</title><creator>Reantragoon, Rangsima</creator><creator>Corbett, Alexandra</creator><creator>Sakala, Isaac</creator><creator>Gherardin, Nicholas</creator><creator>Furness, John</creator><creator>Chen, Zhenjun</creator><creator>Eckle, Sidonia</creator><creator>Uldrich, Adam</creator><creator>Birkinshaw, Richard</creator><creator>Patel, Onisha</creator><creator>Kostenko, Lyudmila</creator><creator>Meehan, Bronwyn</creator><creator>Kedzierska, Katherine</creator><creator>Liu, Ligong</creator><creator>Fairlie, David</creator><creator>Hansen, Ted</creator><creator>Godfrey, Dale</creator><creator>Rossjohn, Jamie</creator><creator>McCluskey, James</creator><creator>Kjer-Nielsen, Lars</creator><subject>Medical and health sciences (11)</subject><publisher>Rockefeller University Press</publisher><date>2013</date><type>text</type><type>journal article</type><identifier linktype="unknown">http://arrow.monash.edu.au/hdl/1959.1/955583</identifier><identifier>monash:126899</identifier><language>eng</language><relation>Journal of Experimental Medicine [P], vol. 210, no. 11, p. 2305-2320</relation><relation>urn:ISSN:00221007</relation><rights>Subscription access to fulltext</rights></dc>
      </metadata><metadataSource type="nuc">VMOU:R</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013</issued><holdingsCount>2</holdingsCount></version><version id="206628597"><record><header>
      <identifier>oai:espace.library.uq.edu.au:UQ:314824</identifier>
      <datestamp>2017-11-11T20:32:12Z</datestamp>
							      <setSpec>oai:espace.library.uq.edu.au:UQ:3858</setSpec>
				      <setSpec>oai:espace.library.uq.edu.au:UQ:283553</setSpec>
			    </header><metadata>
	      <dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	            <title>Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells</title>
	
		





	





	
	
	
        <bibliographicCitation>
        Reantragoon, Rangsima, Corbett, Alexandra J., Sakala, Isaac G., Gherardin, Nicholas A., Furness, John B., Chen, Zhenjun, Eckle, Sidonia B. G., Uldrich, Adam P., Birkinshaw, Richard W., Patel, Onisha, Kostenko, Lyudmila, Meehan, Bronwyn, Kedzierska, Katherine, Liu, Ligong, Fairlie, David P., Hansen, Ted H., Godfrey, Dale I., Rossjohn, Jamie, McCluskey, James and Kjer-Nielsen, Lars (2013) Antigen-loaded MR1 tetramers define T cell receptor heterogeneity in mucosal-associated invariant T cells. Journal of Experimental Medicine, 210 11: 2305-2320. doi:10.1084/jem.20130958
    </bibliographicCitation><relation>http://doi.org/10.1084/jem.20130958
    </relation>
    
	
	
	

			<description>
					Mucosal-associated invariant T cells (MAIT cells) express a semi-invariant T cell receptor (TCR) alpha-chain, TRAV1-2-TRAJ33, and are activated by vitamin B metabolites bound by the major histocompatibility complex (MHC)-related class I-like molecule, MR1. Understanding MAIT cell biology has been restrained by the lack of reagents to specifically identify and characterize these cells. Furthermore, the use of surrogate markers may misrepresent the MAIT cell population. We show that modified human MR1 tetramers loaded with the potent MAIT cell ligand, reduced 6-hydroxymethyl-8-D-ribityllumazine (rRL-6-CH2OH), specifically detect all human MAIT cells. Tetramer(+) MAIT subsets were predominantly CD8(+) or CD4(-)CD8(-), although a small subset of CD4(+) MAIT cells was also detected. Notably, most human CD8(+) MAIT cells were CD8 alpha(+)CD8 beta(-/lo), implying predominant expression of CD8 alpha alpha homodimers. Tetramer-sorted MAIT cells displayed a T(H)1 cytokine phenotype upon antigen-specific activation. Similarly, mouse MR1-rRL-6-CH2OH tetramers detected CD4(+), CD4(-)CD8(-) and CD8(+) MAIT cells in V. 19 transgenic mice. Both human and mouse MAIT cells expressed a broad TCR-beta repertoire, and although the majority of human MAIT cells expressed TRAV1-2-TRAJ33, some expressed TRAJ12 or TRAJ20 genes in conjunction with TRAV1-2. Accordingly, MR1 tetramers allow precise phenotypic characterization of human and mouse MAIT cells and revealed unanticipated TCR heterogeneity in this population.
				</description>
	
        <type>journal article</type>
        <date>2013-10-01</date>
																        <creator>Reantragoon, Rangsima</creator>
							        <creator>Corbett, Alexandra J.</creator>
							        <creator>Sakala, Isaac G.</creator>
							        <creator>Gherardin, Nicholas A.</creator>
							        <creator>Furness, John B.</creator>
							        <creator>Chen, Zhenjun</creator>
							        <creator>Eckle, Sidonia B. G.</creator>
							        <creator>Uldrich, Adam P.</creator>
							        <creator>Birkinshaw, Richard W.</creator>
							        <creator>Patel, Onisha</creator>
							        <creator>Kostenko, Lyudmila</creator>
							        <creator>Meehan, Bronwyn</creator>
							        <creator>Kedzierska, Katherine</creator>
							        <creator>Liu, Ligong</creator>
							        <creator>Fairlie, David P.</creator>
							        <creator>Hansen, Ted H.</creator>
							        <creator>Godfrey, Dale I.</creator>
							        <creator>Rossjohn, Jamie</creator>
							        <creator>McCluskey, James</creator>
							        <creator>Kjer-Nielsen, Lars</creator>
											
																        <subject>Vitamin B Metabolites</subject>
							        <subject>Mait Cells</subject>
							        <subject>Alpha Chain</subject>
							        <subject>Bacterial-Infection</subject>
							        <subject>Recognition</subject>
							        <subject>Lymphocytes</subject>
									        
		

		
		

						        	<publisher>Rockefeller University Press</publisher>
												        			      			      <language>eng</language>
			      					

																		<relation>AI046553</relation>
									


										                            <identifier linktype="fulltext">http://espace.library.uq.edu.au/view/UQ:314824/UQ314824_OA.pdf</identifier>
            							        <identifier linktype="fulltext">http://espace.library.uq.edu.au/view/UQ:314824</identifier>

		
	      </dc>
	




    </metadata><metadataSource type="nuc">QU:IR</metadataSource></record><type>Article</type><type>Article/Journal or magazine article</type><issued>2013-10-01</issued><holdingsCount>1</holdingsCount></version></work></records></zone><zone name="picture"><records s="0" n="0" total="0" /></zone><zone name="book"><records s="0" n="0" total="0" /></zone><zone name="map"><records s="0" n="0" total="0" /></zone><zone name="collection"><records s="0" n="0" total="0" /></zone><zone name="music"><records s="0" n="0" total="0" /></zone></response>
        

Examples

Click on any of the examples below to open them in this console. If you want to use them in your own code you'll need to get an API key and add '&key=[Your API key]' to the url.

See the Trove API documentation for a full list of available parameters and detailed information on constructing queries.

Search everything

Parameters url
  • zone: all
  • q (query): wragge
  • encoding: xml (default)
  • n (number of results): 20 (default)
http://api.trove.nla.gov.au/result?q=wragge&zone=all
  • zone: all
  • q (query): wragge
  • encoding: json
  • n (number of results): 50
http://api.trove.nla.gov.au/result?q=wragge&zone=all&encoding=json&n=50
  • zone: all
  • q (query): nuc:ANL (contributor id)
  • encoding: json
  • n (number of results): 50
http://api.trove.nla.gov.au/result?q=nuc:ANL&zone=all&encoding=json
  • zone: all
  • q (query): wragge
  • encoding: json
  • n (number of results): 20 (default)
  • l-australian: y (in Australia or by Australians)
  • l-availability: y/f (freely accessible online)
http://api.trove.nla.gov.au/result?q=wragge&zone=all&encoding=json&l-australia=y&l-availability=y/f

Search newspapers

Parameters url
  • zone: newspaper
  • q (query): wragge AND weather
  • encoding: json
  • n (number of results): 20 (default)
http://api.trove.nla.gov.au/result?q=wragge+AND+weather&zone=newspaper&encoding=json
  • zone: newspaper
  • q (query): wragge AND weather
  • encoding: json
  • l-year: 1903
  • l-category: Article
  • n (number of results): 20 (default)
http://api.trove.nla.gov.au/result?q=wragge AND weather&zone=newspaper&encoding=json&l-year=1903
  • zone: newspaper
  • q (query): wragge AND weather
  • encoding: json
  • l-decade: 190
  • facet: year
  • n (number of results): 0
http://api.trove.nla.gov.au/result?q=wragge AND weather&zone=newspaper&encoding=json&l-decade=190&facet=year&n=0

Search other zones

Parameters url
  • zone: book,picture
  • q (query): wragge AND weather
  • encoding: json
  • n (number of results): 20 (default)
http://api.trove.nla.gov.au/result?q=wragge AND weather&zone=book,picture&encoding=json
  • zone: book
  • q (query): weather
  • encoding: json
  • l-format: Thesis
  • n (number of results): 20 (default)
http://api.trove.nla.gov.au/result?q=weather&zone=book&encoding=json&l-format=Thesis
  • zone: book
  • q (query): weather
  • encoding: json
  • facet: format
  • n (number of results): 0
http://api.trove.nla.gov.au/result?q=weather&zone=book&encoding=json&facet=format&n=0
  • zone: list
  • q (query): war memorials
  • encoding: json
http://api.trove.nla.gov.au/result?q=war memorials&zone=list&encoding=json

Get record

Parameters url
  • type: newspaper
  • article id: 41697877
  • reclevel: full
  • encoding: json
http://api.trove.nla.gov.au/newspaper/41697877?encoding=json&reclevel=full
  • type: newspaper
  • article id: 146871507
  • reclevel: full
  • include: articletext
http://api.trove.nla.gov.au/newspaper/41697877?reclevel=full&include=articletext
  • type: work
  • article id: 36904481
  • reclevel: full
  • encoding: json
http://api.trove.nla.gov.au/work/36904481?encoding=json&reclevel=full
  • type: work
  • article id: 34769014
  • reclevel: full
  • include: workVersions,holdings
  • encoding: json
http://api.trove.nla.gov.au/work/34769014?encoding=json&include=workVersions,holdings&reclevel=full
  • type: list
  • list id: 1442
  • reclevel: full
  • include: listItems
  • encoding: json
http://api.trove.nla.gov.au/list/1442?encoding=json&reclevel=full&include=listItems

List/get newspaper titles

Parameters url
  • state: vic
http://api.trove.nla.gov.au/newspaper/titles?state=vic
  • title id: 35
  • encoding: json
http://api.trove.nla.gov.au/newspaper/title/35?encoding=json
  • title id: 35
  • include: years
  • encoding: json
http://api.trove.nla.gov.au/newspaper/title/35?encoding=json&include=years

List/get Trove contributors

Parameters url
  • encoding: json
http://api.trove.nla.gov.au/contributor?encoding=json
  • NUC identifier: ANL
  • reclevel: full
  • encoding: json
http://api.trove.nla.gov.au/contributor/ANL?encoding=json&reclevel=full