TRANSPLANT VASCULOPATHY

Transplant vasculopathy constitutes the major impediment to long-term survival in heart transplant recipients. Within the ''response to immu ne injury'' paradigm, it can best be understood as the resultant of an orchestrated recipient immune response to the initial allogenic stimu lus by graft vascular endothelium. This response incorporates the elab oration of complex coordinated cytokine patterns and corresponding cel l types including B-lymphocytes, T-(helper1)- and T-(helper2)-cells, c ytotoxic T-cells, macrophages, and poly morphonuclear cells. These att ack the alloantigenic vascular endothelium and lead, by complex cytoki ne signalling, to migration of donor smooth muscle cells from the medi a into the intima, associated with a switch from the contractile to a synthetic phenotype. In conjunction with recipient T-cells, macrophage s, and lipids, the intimal fibroproliferative growth of the donor vess el is hereby initiated.