Human endothelial cell costimulation of T cell IFN-gamma production
العنوان: | Human endothelial cell costimulation of T cell IFN-gamma production |
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المؤلفون: | D M Briscoe, L E Henault, C Geehan, S I Alexander, A H Lichtman |
المصدر: | The Journal of Immunology. 159:3247-3256 |
بيانات النشر: | The American Association of Immunologists, 1997. |
سنة النشر: | 1997 |
مصطلحات موضوعية: | Immunology, Immunology and Allergy |
الوصف: | In this report, we show that human endothelial cells (EC) provide costimulatory signals to mitogen-activated CD4+ T cells to augment IFN-gamma production. We also show that EC can enhance responsiveness of the T cells to IL-12. While IL-12 has no effect on IFN-gamma production by cultured CD4+ T cells in the absence of EC, addition of IL-12 to T cell-EC cocultures augments IFN-gamma production by as much as fivefold. Separation of T cells from EC by a semipermeable membrane inhibits the effect of EC and IL-12 on IFN-gamma production. Anti-LFA-3 Abs, in the absence or presence of IL-12, inhibit EC costimulation of IFN-gamma production by up to 50%, while Abs to intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), LFA-1, and very late antigen-4 (VLA-4) have relatively little effect. Pretreatment of T cells with conditioned medium from T cell-EC cocultures, or with IL-2 or IL-1 alpha similarly primes CD4+ T cells for the costimulatory effect of IL-12 on IFN-gamma production. EC costimulation of IFN-gamma production is inhibited by cyclosporine. However, in the presence of IL-12 there is a marked resistance to this inhibitory effect, suggesting that the IL-12-induced costimulatory pathway is distinct from the costimulatory pathway activated by endothelium alone. Our data are consistent with the hypothesis that, as a consequence of interactions with endothelium, T cells that migrate into an inflammatory site are primed to have enhanced responses to Ag and cytokine(s), such as IL-12, that influence T cell-cytokine production. |
تدمد: | 1550-6606 0022-1767 |
DOI: | 10.4049/jimmunol.159.7.3247 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::a75f841a44c0c6a13eb341c6d23399d1 https://doi.org/10.4049/jimmunol.159.7.3247 |
رقم الانضمام: | edsair.doi...........a75f841a44c0c6a13eb341c6d23399d1 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15506606 00221767 |
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DOI: | 10.4049/jimmunol.159.7.3247 |