Immunologic aspects of rejection.

Abstract The endothelial cell is a likely candidate for the site of rejection in allograft or xenograft cardiac transplantation. Any or all of the cell surface molecules on donor endothelium could be a site for recipient antibody-mediated lysis. Lymphokines affect a variety of changes on endothelial cells, ranging from changes in cell morphology to the de novo synthesis of HLA antigens, to the expression of endothelium-specific antigens. Increases in free C1q and its subsequent binding to endothelium could cause nonantibody mediated complement activation with subsequent cell lysis. Injury of vascular cells by mediators secreted by anaphylatoxin-activated PMNs or mast cells could lead to endothelial death. A combination of these processes may account for the final organ failure in cardiac transplantation.