rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
9
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pubmed:dateCreated |
2006-8-22
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pubmed:abstractText |
T cells expressing an invariant V(alpha)19-J(alpha)33 T cell receptor alpha-chain (V(alpha)19i TCR) are restricted by the nonpolymorphic major histocompatibility complex class Ib molecule MR1. Whether V(alpha)19i T cells are involved in autoimmunity is not understood. Here we demonstrate that T cells expressing the V(alpha)19i TCR transgene inhibited the induction and progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Similarly, EAE was exacerbated in MR1-deficient mice, which lack V(alpha)19i T cells. EAE suppression was accompanied by reduced production of inflammatory mediators and increased secretion of interleukin 10. Interleukin 10 production occurred at least in part through interactions between B cells and V(alpha)19i T cells mediated by the ICOS costimulatory molecule. These results suggest an immunoregulatory function for V(alpha)19i T cells.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD1,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD1d,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Icos protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Variable Region,
http://linkedlifedata.com/resource/pubmed/chemical/Inducible T-Cell Co-Stimulator...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Mr1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
|
pubmed:issn |
1529-2908
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
7
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
987-94
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16878136-Animals,
pubmed-meshheading:16878136-Antigens, CD1,
pubmed-meshheading:16878136-Antigens, CD1d,
pubmed-meshheading:16878136-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:16878136-B-Lymphocytes,
pubmed-meshheading:16878136-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:16878136-Histocompatibility Antigens Class I,
pubmed-meshheading:16878136-Immunoglobulin Variable Region,
pubmed-meshheading:16878136-Inducible T-Cell Co-Stimulator Protein,
pubmed-meshheading:16878136-Interleukin-10,
pubmed-meshheading:16878136-Lymphocyte Activation,
pubmed-meshheading:16878136-Mice,
pubmed-meshheading:16878136-Mice, Transgenic,
pubmed-meshheading:16878136-Multiple Sclerosis,
pubmed-meshheading:16878136-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:16878136-T-Lymphocytes, Regulatory
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pubmed:year |
2006
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pubmed:articleTitle |
Invariant V(alpha)19i T cells regulate autoimmune inflammation.
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pubmed:affiliation |
Department of Immunology, National Institute of Neuroscience, National Centre of Neurology and Psychiatry, Tokyo 187-8502, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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