In Type II hypersensitivity, tissue damage can occur through multiple effector mechanisms. Which of the following correctly pairs the antibody target with the disease mechanism in Goodpasture syndrome?

• A Anti-GBM antibodies against heparan sulfate proteoglycan → granular immune complex deposition → membranoproliferative pattern
• B Anti-GBM antibodies against α3 chain of type IV collagen → linear IgG deposition → complement activation and neutrophilic destruction of GBM ✓
• C Anti-GBM antibodies against α1 chain of type IV collagen → ADCC by NK cells without complement activation
• D Anti-phospholipase A2 receptor antibodies → podocyte injury → membranous nephropathy

Explanation

Goodpasture syndrome involves autoantibodies directed specifically against the non-collagenous (NC1) domain of the α3 chain of type IV collagen, which is uniquely expressed in glomerular and alveolar basement membranes. The antibodies bind uniformly along the GBM, producing characteristic linear IgG staining by immunofluorescence (as opposed to the granular 'lumpy-bumpy' pattern of immune complex diseases). Complement activation (especially C3b/MAC) and Fc receptor-mediated neutrophil recruitment cause crescentic (rapidly progressive) glomerulonephritis and pulmonary hemorrhage. Anti-PLA2R antibodies cause primary membranous nephropathy — a distinct entity.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.