A 32-year-old woman presents with heat intolerance, weight loss despite increased appetite, and a diffusely enlarged non-tender thyroid. In terms of the Gell and Coombs framework, the hypersensitivity mechanism underlying this disease is best described as:

• A Type II hypersensitivity mediated by antibodies that stimulate a cell surface receptor ✓
• B Type III hypersensitivity with immune complex deposition in the thyroid
• C Type IV hypersensitivity with cytotoxic T cell destruction of follicular cells
• D Type I hypersensitivity with IgE-mediated mast cell degranulation

Explanation

Graves disease is the classic example of a stimulatory type II reaction: autoantibodies against the TSH receptor activate adenylate cyclase constitutively, driving thyroid hormone synthesis and glandular growth without destroying the gland. This distinguishes it from Hashimoto thyroiditis, where type IV mechanisms and cytotoxicity dominate. Type III reactions such as serum sickness involve immune complex deposition, and type I reactions require IgE bound to mast cells, neither of which operates here.

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

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Written and medically reviewed by the StethoPrep medical team.