A 28-year-old woman with SLE develops hemolytic anemia after a viral upper respiratory infection. Direct Coombs test is positive. Complement levels (C3, C4) are low. The hemolysis in this scenario is best explained by which mechanism?
- A Type II hypersensitivity — antibody-dependent complement-mediated lysis of RBCs ✓
- B Type III hypersensitivity — immune complex deposition on RBC membranes
- C Type IV hypersensitivity — cytotoxic T cells recognizing altered RBC antigens
- D Type I hypersensitivity — IgE-mediated mast cell degranulation causing RBC osmotic lysis
Correct answer: A. Type II hypersensitivity — antibody-dependent complement-mediated lysis of RBCs
Explanation
Autoimmune hemolytic anemia in SLE is a classic Type II (cytotoxic) hypersensitivity reaction. IgG or IgM autoantibodies bind directly to RBC surface antigens, activating complement (explaining low C3/C4), leading to intravascular lysis or extravascular hemolysis via Fc receptor-mediated phagocytosis. The direct Coombs test detects antibody or complement bound to the patient's own RBCs. Type III involves circulating immune complexes depositing in tissues; Type IV is cell-mediated and does not involve complement or antibody-coated cells.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.