| pubmed-article:1692079 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C0081942 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C1367475 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:1692079 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:1692079 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:1692079 | pubmed:dateCreated | 1990-6-6 | lld:pubmed |
| pubmed-article:1692079 | pubmed:abstractText | We have demonstrated that endothelial cells (EC) augment IL-2 production by PHA-stimulated PBMC or purified CD4+ T cells and that the increase is apparent both in the amount of soluble IL-2 secreted and in the level of specific mRNA detectable by Northern blot hybridization. The ability of EC to affect levels of IL-2 cannot be reproduced by soluble factors, including the cytokines IL-1, IL-6, IFN-gamma, or TNF, conditioned medium from resting EC or IL-1, IFN-gamma- or TNF-treated EC, or from resting PBMC + EC cultures. Separation of the EC and PBMC by a Transwell membrane demonstrated that cell contact was required for augmentation of IL-2 synthesis and that this effect was unlikely to be mediated by a short-lived soluble signal. The cell-cell interaction required the ligand pair CD2/LFA-3, since augmentation could be inhibited by antibodies to these structures. Antibodies to ICAM-1, LFA-1, CD4, and MHC class II were without effect. A contact-dependent pathway involving CD2/LFA-3 interactions also may be used by EC to augment IL-2 production from T cells stimulated more specifically through the TCR/CD3 complex with antibody OKT3. This pathway provides a proliferative advantage to T cells stimulated with OKT3 in the presence of EC and may also be involved in the proliferative response of resting T cells to allogeneic class II MHC-expressing EC. We propose that EC augmentation of T cell IL-2 synthesis may be critical in the ability of EC to elicit primary T cell antigen responses and may have consequences for the development of localized cell-mediated immune reactions. | lld:pubmed |
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| pubmed-article:1692079 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1692079 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1692079 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1692079 | pubmed:month | May | lld:pubmed |
| pubmed-article:1692079 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:1692079 | pubmed:author | pubmed-author:HughesC CCC | lld:pubmed |
| pubmed-article:1692079 | pubmed:author | pubmed-author:PoberJ SJS | lld:pubmed |
| pubmed-article:1692079 | pubmed:author | pubmed-author:SavageC OCO | lld:pubmed |
| pubmed-article:1692079 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1692079 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1692079 | pubmed:volume | 171 | lld:pubmed |
| pubmed-article:1692079 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1692079 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1692079 | pubmed:pagination | 1453-67 | lld:pubmed |
| pubmed-article:1692079 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1692079 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:1692079 | pubmed:articleTitle | Endothelial cells augment T cell interleukin 2 production by a contact-dependent mechanism involving CD2/LFA-3 interaction. | lld:pubmed |
| pubmed-article:1692079 | pubmed:affiliation | Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115. | lld:pubmed |
| pubmed-article:1692079 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1692079 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1692079 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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