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

• A Preformed recipient antibodies (anti-HLA or anti-ABO) activating complement and causing vascular thrombosis ✓
• B T-cell-mediated cytotoxicity (CD8+ CTLs)
• C NK cell infiltration and innate immune activation
• D Regulatory T-cell failure permitting Th17 activation

Explanation

Hyperacute rejection is caused by preformed antibodies in the recipient (anti-donor ABO blood group antibodies or preformed anti-HLA antibodies from prior sensitization — previous transplant, transfusion, or pregnancy) that bind immediately to donor endothelium, activating complement and coagulation cascades, causing widespread microvascular thrombosis, ischemia, and irreversible graft failure within minutes to hours. It is prevented by ABO compatibility testing and pre-transplant lymphocyte crossmatch. Acute rejection (days to weeks) is T-cell mediated; chronic rejection involves both antibody-mediated and cellular mechanisms.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.