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Lymphocyte-endothelial interactions and tolerance induction.

It is now apparent that mAb to a growing number of intracellular adhesion molecules can not only promote allograft survival but also stimulate allogeneic tolerance in rodent transplant models. Intracellular adhesion molecules are responsible for a variety of immune functions, including proper lymphocyte migration and productive lymphocyte activation. Vascular endothelial cells have carefully regulated expression of adhesion molecules, which they use to control the homeostatic and inflammatory patterns of lymphocyte trafficking. This leads to the hypothesis that an impairment of lymphocyte trafficking by anti-adhesion molecules mAb results in prolonged allograft survival and/or allogeneic tolerance. In the broader view, endothelial cells belong to a small group of cell types that can serve as APC to T cells, and this APC function is strongly influenced by adhesion molecules. This leads to the hypothesis that an impairment of APC function by anti-adhesion molecule mAb results in allograft survival and allogeneic tolerance. The two hypotheses are not mutually exclusive, and both need to be tested. In general, however, it appears that intracellular adhesion molecules are intimately involved not only in the mechanisms of graft-induced alloactivation and but also in the mechanisms of allogeneic tolerance induction by virtue of their essential role in lymphocyte-endothelial and/or lymphocyte-APC interactions.