A patient receiving a kidney transplant develops acute antibody-mediated rejection within 1 week despite negative pre-transplant crossmatch. Biopsy shows C4d deposition in peritubular capillaries. The primary effector mechanism responsible for this injury is:

• A CD8+ cytotoxic T cell recognition of donor MHC class I molecules
• B NK cell ADCC mediated by pre-formed anti-HLA antibodies
• C Th17-driven neutrophil infiltration independent of complement
• D De novo donor-specific antibodies (DSAs) activating complement via classical pathway ✓

Explanation

C4d is a split product of complement C4 that covalently binds to endothelium after classical pathway activation by antibody-antigen complexes; its peritubular capillary deposition is diagnostic of antibody-mediated rejection (AMR). De novo DSAs generated against donor HLA antigens activate complement, leading to endothelial damage. CD8+ T cells mediate acute cellular rejection without C4d deposition. NK-cell ADCC via ADCC requires pre-formed antibodies but C4d deposition specifically indicates classical pathway complement activation.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.