Release of endothelial cell-associated heparan sulfate proteoglycan by activated T cells

The histopathology of cellular rejection is characterized by the infiltration of mononuclear cells into the transplanted organ, interstitial edema, and, in severe cases, hemorrhage and thrombosis. These findings suggest that the pathophysiology of rejection might involve an impairment of the barrier and anticoagulant functions of blood vessel endothelium. One potential cause of endothelial cell dysfunction is structural damage or lysis mediated by activated lymphocytes or by the cytokines they release. The decrease in expression of some endothelial cell antigens is strong evidence of such damage. However, the histology of rejecting allografts provides little evidence of lysis of endothelial cells. Furthermore, the increased expression of such endothelial antigens as intercellular adhesion molecule-1 and vascular cell adhesion molecule in allograft rejection and the rapid improvement sometimes seen with the institution of immunosuppressive therapy indicate that despite structural changes as may occur, endothelial cells in a rejecting graft remain viable and metabolically active.