Graves disease is classified under which Gell and Coombs type of hypersensitivity, and what is its characteristic effector mechanism?
- A Type IVa, Th1 mediated macrophage activation against thyrocytes
- B Type III, immune complex deposition within the thyroid gland
- C Type II, antibody-mediated stimulation of a cell surface receptor ✓
- D Type V does not exist; Graves disease is type IVb cytotoxic T cell mediated
Explanation
Graves disease is the classic example of stimulating type II hypersensitivity. Autoantibodies bind the TSH receptor on follicular epithelial cells and mimic TSH action, driving unregulated hormone synthesis and secretion independent of pituitary feedback. Unlike myasthenia gravis, where antibody blocks the acetylcholine receptor, here the antibody activates the receptor, so gland destruction is absent and the thyroid is diffusely hypertrophied. Complement-mediated lysis is not involved because the antibody is stimulatory.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
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