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rdf:type |
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lifeskim:mentions |
umls-concept:C0004364,
umls-concept:C0039198,
umls-concept:C0085358,
umls-concept:C0441655,
umls-concept:C0851285,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1512900,
umls-concept:C1704675,
umls-concept:C1706438,
umls-concept:C2698600,
umls-concept:C2699488
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pubmed:issue |
49
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pubmed:dateCreated |
2008-12-10
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pubmed:abstractText |
Regulation of autoreactive CD4 T cells is essential to maintain self-tolerance and prevent autoimmune disease. Although CD8 T regulatory (Treg) cells that recognize self-peptides restricted by Qa-1 (HLA-E in humans) inhibit autoreactive CD4 cells and attenuate experimental autoimmune encephalomyelitis (EAE), the mechanism of this interaction is unclear. We generated Qa-1 mutant knock-in mice that impair Qa-1 binding to the T cell receptor (TCR) and CD94/NKG2A receptors. Analysis of these mice showed that TCR-dependent recognition of Qa-1-peptide complexes on target CD4 cells is essential for suppression by CD8 Treg cells. Further analysis revealed that genetic disruption of the Qa-1-CD94/NKG2A interaction unleashes robust CD8 Treg cell activity that completely abolishes development of EAE.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-10854647,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-11169442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-11812997,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-12732654,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-12824465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-15039756,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-15098030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-15135634,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-15520848,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-15520850,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-16903903,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-16903905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-17509909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-18077361,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-18234356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-7830771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-8808679,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-9539772,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-9551889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19047627-9815261
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1091-6490
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
9
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pubmed:volume |
105
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
19420-5
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:19047627-Adoptive Transfer,
pubmed-meshheading:19047627-Animals,
pubmed-meshheading:19047627-Autoimmunity,
pubmed-meshheading:19047627-CD8-Positive T-Lymphocytes,
pubmed-meshheading:19047627-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:19047627-Gene Knock-In Techniques,
pubmed-meshheading:19047627-Histocompatibility Antigens Class I,
pubmed-meshheading:19047627-Immune Tolerance,
pubmed-meshheading:19047627-Mice,
pubmed-meshheading:19047627-Mice, Inbred C57BL,
pubmed-meshheading:19047627-Mice, Transgenic,
pubmed-meshheading:19047627-NK Cell Lectin-Like Receptor Subfamily C,
pubmed-meshheading:19047627-NK Cell Lectin-Like Receptor Subfamily D,
pubmed-meshheading:19047627-Perforin,
pubmed-meshheading:19047627-T-Lymphocytes, Regulatory
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pubmed:year |
2008
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pubmed:articleTitle |
Regulation of CD8+ regulatory T cells: Interruption of the NKG2A-Qa-1 interaction allows robust suppressive activity and resolution of autoimmune disease.
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pubmed:affiliation |
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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