In solid organ transplantation, the principal mechanism of hyperacute rejection occurring within minutes to hours of reperfusion is:
- A CD8+ T-cell mediated cytotoxicity directed against donor HLA class I antigens
- B Preformed recipient antibodies (predominantly anti-HLA or anti-ABO) activating complement and coagulation in the graft vasculature ✓
- C NK cell-mediated killing of donor endothelium lacking self-HLA expression
- D Macrophage infiltration and release of TNF-α causing endothelial apoptosis
Explanation
Hyperacute rejection is caused by preformed recipient antibodies — primarily anti-ABO blood group antibodies or anti-HLA donor-specific antibodies (DSA) — that bind to donor vascular endothelium immediately upon reperfusion. This triggers complement activation (classical pathway), endothelial injury, platelet aggregation, and intravascular thrombosis, leading to irreversible graft loss within minutes to hours. Cross-match testing before transplantation prevents this by detecting preformed anti-HLA DSA. Cell-mediated mechanisms cause acute (days to weeks) or chronic rejection.
Reference: Bailey & Love's Short Practice of Surgery, 27th ed.
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Written and medically reviewed by the StethoPrep medical team.