| pubmed-article:7684325 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7684325 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:7684325 | lifeskim:mentions | umls-concept:C0078056 | lld:lifeskim |
| pubmed-article:7684325 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:7684325 | lifeskim:mentions | umls-concept:C1332709 | lld:lifeskim |
| pubmed-article:7684325 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:7684325 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:7684325 | pubmed:dateCreated | 1993-6-22 | lld:pubmed |
| pubmed-article:7684325 | pubmed:abstractText | Optimal stimulation of CD4+ T cells in an immune response requires not only signals transduced via the CD3/TCR complex but also costimulatory signals delivered as a consequence of interactions between T-cell surface-associated costimulatory R and their counter-R on APC. CD28 plays a crucial role as a dominant costimulatory R during the induction of CD4+ T-cell proliferation by interacting with counter-R B7 on APC to sustain IL-2 production. The absence of CD28-mediated costimulation has been postulated to result in T-cell anergy or unresponsiveness. The costimulatory effects of CD28 can be generated with its natural counter-R B7 or mAb directed at CD28. Using soluble C gamma 1 chimeras of B7, ICAM-1, and VCAM-1, we have recently shown that B7 costimulates TCR-dependent proliferation of Ag-primed CD4+ T cells more efficiently than that of resting nonactivated CD4+ T cells. In contrast, proliferation of resting CD4+ T cells can be efficiently costimulated by either ICAM-1 or VCAM-1 via interactions with their R CD11a/CD18 (LFA-1/beta 2 integrin) and CD29/CD49d (VLA-4/beta 1 integrin), respectively. TCR-directed preactivation of resting CD4+ T cells with ICAM-1 can induce increased responsiveness to B7 costimulation. In this study, we show that prior TCR-directed activation of resting CD4+ T cells with VCAM-1 induced increased responsiveness to B7 costimulation. VCAM-1 also synergized with B7 to bring about supraoptimal proliferation of CD4+ T cells. In addition, costimulation of resting T cells with VCAM-1 significantly increased not only surface expression of CD28 but also CD28-mediated mobilization of intracellular free [Ca2+]i. Similar activation of T cells with fibronectin also resulted in increased B7 responsiveness, suggesting the involvement of VLA-4 molecule. VCAM-1 costimulation induced hyperresponsiveness to B7 costimulation in both CD18+ (normal) and CD18- (leukocyte adhesion deficient) T cells. Thus, VCAM-1 may play an important costimulatory role during the activation of resting T cells and, by augmenting responsiveness to B7, facilitate optimal development of immunological memory in addition to various regulatory and effector functions. | lld:pubmed |
| pubmed-article:7684325 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7684325 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7684325 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:7684325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7684325 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7684325 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:7684325 | pubmed:issn | 0008-8749 | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:OchsH DHD | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:LinsleyP SPS | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:DamleN KNK | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:LedbetterJ... | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:AruffoAA | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:KlussmanKK | lld:pubmed |
| pubmed-article:7684325 | pubmed:author | pubmed-author:LeytzeGG | lld:pubmed |
| pubmed-article:7684325 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7684325 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7684325 | pubmed:volume | 148 | lld:pubmed |
| pubmed-article:7684325 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7684325 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7684325 | pubmed:pagination | 144-56 | lld:pubmed |
| pubmed-article:7684325 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
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| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:meshHeading | pubmed-meshheading:7684325-... | lld:pubmed |
| pubmed-article:7684325 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:7684325 | pubmed:articleTitle | Costimulation via vascular cell adhesion molecule-1 induces in T cells increased responsiveness to the CD28 counter-receptor B7. | lld:pubmed |
| pubmed-article:7684325 | pubmed:affiliation | Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, Washington 98121. | lld:pubmed |
| pubmed-article:7684325 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7684325 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:7684325 | pubmed:publicationType | In Vitro | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:7684325 | lld:pubmed |
