pubmed-article:9209493 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0521009 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0003241 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0206527 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1299583 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0221117 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1608386 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1549571 | lld:lifeskim |
pubmed-article:9209493 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
pubmed-article:9209493 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:9209493 | pubmed:dateCreated | 1997-7-22 | lld:pubmed |
pubmed-article:9209493 | pubmed:abstractText | V7 is a novel cell surface glycoprotein that is expressed on 25% of circulating T lymphocytes. This molecule appears to play a critical role in T cell activation based on the observation that a monoclonal anti-V7 antibody inhibits T cell receptor (TCR)-dependent interleukin-2 (IL-2) production and proliferation of T cells. In the current study, CD4+ V7+ and CD4+ V7- T cells were separated from one another and their response to various stimuli analyzed. Although there were only minor differences between the two subsets in the expression of activation/differentiation markers, including CD45RA and R0 isotypes, when exposed to immobilized anti-CD3 or anti-TCR antibodies in the absence of APC, CD4+ V7+ T cells alone produced IL-2 and proliferated vigorously. By contrast, CD4+ V7- cells responded poorly to such stimuli, but they recovered their capacity to respond if antigen-presenting cells (APC) or anti-CD28-antibody were added to the cultures. The enhancement of the V7- T cell response by APC appears to be related to augmentation of TCR signals because the effect could be blocked by antibodies against molecules on APC [major histocompatibility (MHC) class II, CD86] that are known to up-regulate such signals through their interaction with counter-receptors on T cells. To assess the role of V7 in a system independent of co-stimulation, CD4+ T cells were stimulated with the bacterial superantigens, staphylococcal enterotoxins A and B. The cells responded by proliferating and then becoming anergic. Addition of anti-V7 antibody at the initiation of culture with superantigen did not inhibit cellular proliferation but prevented T cells from becoming anergic, while addition of anti-CD28 antibody had no effect on either proliferation or anergy induction. These results indicate that V7 and CD28 mediate distinct intracellular signals and suggest that V7 functions to preserve T cell reactivity whether the stimulus is mitogenic or anergizing. | lld:pubmed |
pubmed-article:9209493 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:language | eng | lld:pubmed |
pubmed-article:9209493 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9209493 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9209493 | pubmed:month | Jun | lld:pubmed |
pubmed-article:9209493 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:9209493 | pubmed:author | pubmed-author:EnglemanE GEG | lld:pubmed |
pubmed-article:9209493 | pubmed:author | pubmed-author:RivasAA | lld:pubmed |
pubmed-article:9209493 | pubmed:author | pubmed-author:SoaresL RLR | lld:pubmed |
pubmed-article:9209493 | pubmed:author | pubmed-author:RueggCC | lld:pubmed |
pubmed-article:9209493 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9209493 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:9209493 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9209493 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9209493 | pubmed:pagination | 1413-21 | lld:pubmed |
pubmed-article:9209493 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:9209493 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9209493 | pubmed:articleTitle | Differential response of CD4+ V7+ and CD4+ V7- T cells to T cell receptor-dependent signals: CD4+ V7+ T cells are co-stimulation independent and anti-V7 antibody blocks the induction of anergy by bacterial superantigen. | lld:pubmed |
pubmed-article:9209493 | pubmed:affiliation | Department of Pathology, Stanford University School of Medicine, CA 94305, USA. | lld:pubmed |
pubmed-article:9209493 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9209493 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9209493 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |