A 32-year-old woman develops fever, urticaria, lymphadenopathy, and polyarthralgia 10 days after receiving horse antithymocyte globulin for aplastic anemia. Serum complement levels are low. Which mechanism best explains this clinical picture?
- A Preformed IgE antibodies crosslinking mast cell Fc epsilon RI receptors
- B Cytotoxic IgG antibodies directed against cell surface antigens
- C Deposition of soluble immune complexes in vessel walls and tissues with complement activation ✓
- D Sensitized CD4+ Th1 cells releasing IFN-gamma and recruiting macrophages
Correct answer: C. Deposition of soluble immune complexes in vessel walls and tissues with complement activation
Explanation
This is serum sickness, a classic Type III hypersensitivity reaction. Foreign horse proteins act as antigens, host IgG antibodies form immune complexes that deposit in tissues, activate complement (causing low C3/C4), and recruit neutrophils. The 7-14 day latency matches the time needed for antibody production. Option A describes Type I anaphylaxis which is immediate. Option B describes Type II cytotoxic reactions. Option D describes Type IV delayed hypersensitivity.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.