Adhesion and transendothelial migration of mononuclear cells from the circulation into the tissues is the first cellular event in inflammation and immunity/1. The number and specificity of cells recruited to inflammatory sites is spatially and temporally controlled by the expression of a repertoire of adhesion molecules on endothelial cells. In animal models of arthritis induced by either Borrelia burgdorferi or antigenic challenge, endothelial adhesion molecules play a critical role in pathogenesis of joint disease/234. In order to study the role of endothelial cells immunity and how endothelial adhesion molecules, previously thought to be involved only in inflammation, are involved in immunological responses, we have mononuclear cells from heart transplant recipients for 15 minutes/5. In this case the recipient mononuclear cells (which have been primed in vivo to antigenic epitopes present on the endothelial cells) specifically which interact with CD8+(cytotoxic/suppressor) lymphocytes/6. Lymphocytes recognize and are activated by the endothelial class I HLA molecules and activate CD18 dependent integrins which interact with intercellular adhesion molecule-1(ICAM-1)7. Lymphocytes then cause monocyte adhesion/5 which is due to the translocation of p-selectin on the endothelial surface/8. The activation of p-selectin appears to result from interaction with the combination of endothelial class I HLA and a B7 lymphocyte costimulatory molecule/9. Donor or graft specific adhesion is followed by enhanced transendothelial migration into graft specific artery wall endothelial/smooth muscle cell cocultures/10.
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