| pubmed-article:7678619 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C0206527 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C1332709 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
| pubmed-article:7678619 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
| pubmed-article:7678619 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:7678619 | pubmed:dateCreated | 1993-2-22 | lld:pubmed |
| pubmed-article:7678619 | pubmed:abstractText | Staphylococcal enterotoxins, also known as superantigens (SAg), bind class II MHC molecules on APC and upon direct cell-to-cell contact stimulate proliferation of T cells expressing appropriate V beta gene products. The T cell surface molecule CD28 binds its costimulatory counter-receptor, B7 expressed on APC, and augments IL-2 production and T cell growth. Although the role of B7 costimulation during Ag-specific responses of T cells is established, its involvement during the activation of T cells with SAg has not been examined. Using a soluble Ig C gamma 1 chimera of CTLA-4, a second receptor for B7 and a homologue of CD28, this study examines the role of B7 expressed on APC during the induction of proliferation of CD4+ T cells upon stimulation with SAg (SAg/staphylococcal enterotoxins). CTLA-4lg, which has a higher avidity for B7 than CD28, had no effect on the synthesis of IL-2 as well as proliferative responses of CD4+ T cells induced by SAg presented on allogeneic EBV-transformed B cells, and IFN-gamma-activated endothelial cells. In contrast, T cell proliferation induced by alloAg presentation by the same APC was significantly inhibited by CTLA-4lg. mAb directed at the CD11a/CD18 molecule inhibited both SAg-induced and alloAg-induced proliferation of T cells. AlloAg-primed CD4+ T cells, which expressed both class II MHC and intercellular adhesion molecule-1 but not B7, presented SAg to and induced proliferation of both resting and SAg-primed T cells. These responses were inhibited by mAb directed at CD11a/CD18 but not by CTLA-4 Rg. These results suggest that SAg-induced responses differ from those induced by alloAg in that they are not obligatorily dependent on the costimulation by B7. In contrast, adhesive interaction between CD11a/CD18 on T cells and its counter-receptor on SAg-presenting cells is necessary and probably sufficient to support SAg-induced proliferation of T cells. | lld:pubmed |
| pubmed-article:7678619 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7678619 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7678619 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:7678619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:7678619 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7678619 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:7678619 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:7678619 | pubmed:author | pubmed-author:LinsleyP SPS | lld:pubmed |
| pubmed-article:7678619 | pubmed:author | pubmed-author:DamleN KNK | lld:pubmed |
| pubmed-article:7678619 | pubmed:author | pubmed-author:KlussmanKK | lld:pubmed |
| pubmed-article:7678619 | pubmed:author | pubmed-author:LeytzeGG | lld:pubmed |
| pubmed-article:7678619 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7678619 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:7678619 | pubmed:volume | 150 | lld:pubmed |
| pubmed-article:7678619 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7678619 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7678619 | pubmed:pagination | 726-35 | lld:pubmed |
| pubmed-article:7678619 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:7678619 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:7678619 | pubmed:articleTitle | Proliferation of human T lymphocytes induced with superantigens is not dependent on costimulation by the CD28 counter-receptor B7. | lld:pubmed |
| pubmed-article:7678619 | pubmed:affiliation | Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121. | lld:pubmed |
| pubmed-article:7678619 | pubmed:publicationType | Journal Article | lld:pubmed |
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