Clinical meaning
Transplant rejection occurs when the recipient's immune system recognizes donor organ tissue as foreign (non-self) through human leukocyte antigen (HLA) mismatches and mounts an immune response to destroy the graft. Hyperacute rejection occurs within minutes to hours due to pre-formed antibodies against donor HLA antigens, causing immediate vascular thrombosis and graft necrosis. Acute rejection occurs days to months post-transplant through T-cell mediated (cellular) or antibody-mediated (humoral) mechanisms, presenting with organ-specific dysfunction. Chronic rejection develops over months to years through progressive vascular changes, interstitial fibrosis, and gradual organ dysfunction. Prevention requires lifelong immunosuppressive therapy, typically a calcineurin inhibitor (tacrolimus or cyclosporine), an antiproliferative agent (mycophenolate), and corticosteroids. Balancing rejection prevention with infection and malignancy risk from immunosuppression is the central challenge of transplant care.
Exam relevance
Risk factors: - Non-compliance with immunosuppressive medication regimen - Insufficient immunosuppression (subtherapeutic drug levels) - Multiple HLA mismatches between donor and recipient - Prior sensitization from previous transplants, transfusions, or pregnancies - Infection triggering immune activation that cross-reacts with graft