A 25-year-old woman develops serum sickness 8 days after receiving horse antithymocyte globulin (ATG) for aplastic anemia. She develops fever, urticaria, arthralgias, and proteinuria. The immunopathological mechanism involves:
- A IgE sensitization and mast cell degranulation (Type I hypersensitivity)
- B Cytotoxic T-cell destruction of cells bearing foreign antigen (Type IV hypersensitivity)
- C Immune complex (IgG-antigen) deposition in vessel walls activating complement (Type III hypersensitivity) ✓
- D Complement-fixing IgG binding to foreign protein on cell surfaces (Type II hypersensitivity)
Explanation
Serum sickness is the prototypical Type III (immune complex-mediated) hypersensitivity. Antibodies formed against the foreign protein (horse ATG) form soluble immune complexes with circulating antigen 7-10 days after exposure. These complexes deposit in vessel walls, synovium, and glomeruli, fixing complement and triggering C3a/C5a-mediated neutrophil recruitment, releasing proteases and reactive oxygen species causing vasculitis, arthritis, and glomerulonephritis. Low serum C3/C4 and elevated anti-horse protein antibodies confirm the diagnosis. It is self-limited but managed with antihistamines and corticosteroids.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.