| Autor: |
Westphal, J. R., Willems, H. W., Tax, W. J. M., Koene, R. A. P., Ruiter, D. J., De Waal, R. M. W. |
| Předmět: |
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| Zdroj: |
Scandinavian Journal of Immunology; Nov1993, Vol. 38 Issue 5, p435-444, 10p |
| Abstrakt: |
T-cell activation requires not only T-cell receptor (TCR) engagement and subsequent TCR/CD3 cross-linking, but also one or more secondary activation signals generated by accessory cells (AC). We investigated the accessory function of endothelial cells (EC) in an in vitro model for T-cell activation where the first cross-linking signal was delivered to peripheral human T lymphocytes by either immobilized anti- CD3 monoclonal antibody (MoAb) or by PHA. In a previous report, we showed that EC provided a potent costimulatory signal by this model system. We have now analysed the nature of the EC-derived costimulatory signal by testing whether EC could be substituted by cytokines. by studying the effect of EC fixation and by testing the involvement ofa number of adhesion molecules. Our findings indicate that EC accessory function is mediated mainly by membrane-bound factors. The nature of these membrane-bound factors was analysed by studying the inhibitory properties of a series of MoAbs directed against several adhesion molecules. Antibodies directed against CD44. E-selectin, CD31, CD26, B7/BB1, VLA-4 or VCAM-1 were not inhibitory. However, an inhibition, was clearly observed with antibodies against LFA-1 and CD2. Remarkably, this inhibition was not found with MoAbs to their respective counterstructures ICAM-1 and LFA-3. In summary, we postulate that both LFA-l/ICAM-1, and CD2/LFA-3 interactions are involved in EC accessory function, although the role of the EC-associated adhesion partners is not fully understood. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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