Source:http://linkedlifedata.com/resource/pubmed/id/16909431
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2006-9-7
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pubmed:abstractText |
Recent evidence suggests that the functional status of T cells activated independently from their TCR differs substantially from classical MHC-restricted T cells. Here, we show that TCR-independent, short-term stimulation via the common gamma-chain of the IL-2/IL-15 receptor induces non-MHC-restricted cytotoxicity and sustained cytokine secretion in purified CD4+ or CD8+ T cells. NK-like cytotoxicity is directed against MHC class I-negative targets and can be inhibited by classical and non-classical HLA class I molecules. Known inhibitory receptors, such as CD85j (ILT2) and leukocyte-associated Ig-like receptor-1, are not responsible for this HLA-mediated inhibition. NK-like cytotoxicity can be costimulated by NKG2D (CD314) triggering, but 2B4 (CD244) and DNAM-1 (CD226) are not involved. NK-like T cells display an activated phenotype and secrete various cytokines, including IFN-gamma, TNF-alpha, IL-5, IL-13 and MIP-1beta. Under normal conditions, HLA class I-mediated inhibition may function as a safety mechanism to prevent unbalanced cytokine production and effector killing mechanisms by T cells that were activated independently from their TCR. Non-MHC-restricted activity represents a functional status rather than a property of distinct T cell subpopulations. Thus, cytokine-induced, non-MHC-restricted T cells may be relevant in immune responses against tumors showing aberrant MHC expression through their capacities of cytokine production and direct tumor cell eradication.
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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/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/KLRK1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Natural Killer Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
36
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2347-58
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16909431-Cytokines,
pubmed-meshheading:16909431-Cytotoxicity, Immunologic,
pubmed-meshheading:16909431-Histocompatibility Antigens Class I,
pubmed-meshheading:16909431-Humans,
pubmed-meshheading:16909431-Lymphocyte Activation,
pubmed-meshheading:16909431-Major Histocompatibility Complex,
pubmed-meshheading:16909431-NK Cell Lectin-Like Receptor Subfamily K,
pubmed-meshheading:16909431-Receptors, Antigen, T-Cell,
pubmed-meshheading:16909431-Receptors, Immunologic,
pubmed-meshheading:16909431-Receptors, Interleukin-2,
pubmed-meshheading:16909431-Receptors, Natural Killer Cell,
pubmed-meshheading:16909431-T-Lymphocytes
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pubmed:year |
2006
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pubmed:articleTitle |
TCR-independent cytokine stimulation induces non-MHC-restricted T cell activity and is negatively regulated by HLA class I.
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pubmed:affiliation |
Institute of Molecular Immunology, GSF National Research Center for Environment and Health, Munich, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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