In solid organ transplantation, hyperacute rejection occurs within minutes to hours of reperfusion. What is the immunological mechanism?

• A T-cell-mediated cytotoxicity against donor MHC antigens
• B Natural killer cell-mediated lysis of donor endothelium
• C Dendritic cell priming of recipient CD4+ T-cells against donor peptides
• D Pre-formed recipient antibodies against donor HLA or ABO antigens activating complement and causing microvascular thrombosis ✓

Explanation

Hyperacute rejection is mediated by pre-formed recipient antibodies (IgG or IgM) directed against donor ABO blood group antigens or donor HLA class I antigens on vascular endothelium. These antibodies activate the classical complement pathway causing endothelial damage, platelet aggregation, and microvascular thrombosis, leading to rapid graft infarction. It is prevented by ABO compatibility and pre-transplant crossmatch testing. Acute rejection (days to weeks) involves T-cell-mediated mechanisms. Chronic rejection involves antibody-mediated fibrosis and intimal hyperplasia over months to years.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

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