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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6921
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pubmed:dateCreated |
2003-1-23
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pubmed:abstractText |
The immune system must distinguish not only between self and non-self, but also between innocuous and pathological foreign antigens to prevent unnecessary or self-destructive immune responses. Unresponsiveness to harmless antigens is established through central and peripheral processes. Whereas clonal deletion and anergy are mechanisms of peripheral tolerance, active suppression by T-regulatory 1 (Tr1) cells has emerged as an essential factor in the control of autoreactive cells. Tr1 cells are CD4+ T lymphocytes that are defined by their production of interleukin 10 (IL-10) and suppression of T-helper cells; however, the physiological conditions underlying Tr1 differentiation are unknown. Here we show that co-engagement of CD3 and the complement regulator CD46 in the presence of IL-2 induces a Tr1-specific cytokine phenotype in human CD4+ T cells. These CD3/CD46-stimulated IL-10-producing CD4+ cells proliferate strongly, suppress activation of bystander T cells and acquire a memory phenotype. Our findings identify an endogenous receptor-mediated event that drives Tr1 differentiation and suggest that the complement system has a previously unappreciated role in T-cell-mediated immunity and tolerance.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD46,
http://linkedlifedata.com/resource/pubmed/chemical/CD46 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0028-0836
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
23
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pubmed:volume |
421
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
388-92
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12540904-Antigens, CD,
pubmed-meshheading:12540904-Antigens, CD3,
pubmed-meshheading:12540904-Antigens, CD46,
pubmed-meshheading:12540904-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12540904-Cell Differentiation,
pubmed-meshheading:12540904-Cell Division,
pubmed-meshheading:12540904-Cells, Cultured,
pubmed-meshheading:12540904-Flow Cytometry,
pubmed-meshheading:12540904-Humans,
pubmed-meshheading:12540904-Immune Tolerance,
pubmed-meshheading:12540904-Interferon-gamma,
pubmed-meshheading:12540904-Interleukin-10,
pubmed-meshheading:12540904-Interleukin-12,
pubmed-meshheading:12540904-Interleukin-2,
pubmed-meshheading:12540904-Interleukin-4,
pubmed-meshheading:12540904-Lymphocyte Activation,
pubmed-meshheading:12540904-Membrane Glycoproteins,
pubmed-meshheading:12540904-Phenotype,
pubmed-meshheading:12540904-Transforming Growth Factor beta
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pubmed:year |
2003
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pubmed:articleTitle |
Activation of human CD4+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype.
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pubmed:affiliation |
Division of Rheumatology, Washington University School of Medicine, St Louis, Missouri 63110, USA.
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pubmed:publicationType |
Journal Article
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