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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1995-4-26
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pubmed:abstractText |
CD8+ T cells control immune responses, and recent studies suggest that this regulation is, in part, specifically directed towards TCR structures expressed by CD4+ cells. To develop a system to study the role of the TCR in regulatory interactions, we isolated clones of CD4+ cells expressing identified TCR V beta chains. These CD4+ clones were used to stimulate and expand autologous CD8+ cells, which kill the inducing CD4+ clone as well as independently isolated autologous CD4+ clones sharing the same TCR V beta as the inducing cell but not CD4+ T cells expressing different V beta TCRs. This V beta-specific cytotoxicity is dependent on the state of activation of the target cells and is not inhibited by an anti-class I monoclonal antibody, W6/32. We envision that V beta-specific CD8+ T cells of this type may regulate immune responses by direct interaction with antigen-activated CD4+ cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1074-7613
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
177-84
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7895174-CD4-Positive T-Lymphocytes,
pubmed-meshheading:7895174-CD8-Positive T-Lymphocytes,
pubmed-meshheading:7895174-Cytotoxicity, Immunologic,
pubmed-meshheading:7895174-Humans,
pubmed-meshheading:7895174-Lymphocyte Activation,
pubmed-meshheading:7895174-Receptors, Antigen, T-Cell,
pubmed-meshheading:7895174-T-Lymphocyte Subsets
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pubmed:year |
1995
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pubmed:articleTitle |
Human CD8+ T lymphocyte clones specific for T cell receptor V beta families expressed on autologous CD4+ T cells.
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pubmed:affiliation |
Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, New York 10032.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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