In solid organ transplantation, hyperacute rejection occurs within minutes to hours of reperfusion. The immunological mechanism responsible is:

• A CD4+ T-cell-mediated delayed hypersensitivity reaction against donor MHC II antigens
• B Pre-formed recipient antibodies (anti-ABO or anti-HLA IgG) binding to graft endothelium, activating complement and causing intravascular thrombosis ✓
• C NK cell-mediated lysis of donor cells lacking self MHC class I
• D Cytokine-mediated acute tubular necrosis from ischaemia-reperfusion injury

Explanation

Hyperacute rejection is mediated by pre-formed recipient antibodies — typically anti-ABO blood group antibodies or anti-HLA IgG antibodies from prior sensitisation (pregnancy, transfusion, previous transplant). These antibodies bind to donor endothelial antigens, activate complement (C3a, C5a, membrane attack complex), and cause intravascular thrombosis, platelet aggregation, and ischaemic infarction of the graft within minutes to hours. It is virtually prevented by pre-transplant cross-matching and ABO compatibility testing. T-cell mediated processes are responsible for acute (days–weeks) and 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.