A 32-year-old woman has heat intolerance, weight loss, exophthalmos, and pretibial myxedema. Thyroid stimulation persists despite pituitary TSH being fully suppressed. The hypersensitivity mechanism underlying this disease is best described as:

• A Type I hypersensitivity mediated by IgE on thyroid follicular mast cells
• B Type IV hypersensitivity mediated by CD8+ T cell destruction of follicles
• C Type III hypersensitivity with immune complex deposition in the thyroid stroma
• D Type II hypersensitivity with antibody acting as an agonist at a cell surface receptor ✓

Explanation

Graves disease is a classic example of Type II hypersensitivity in which autoantibodies bind the TSH receptor and mimic TSH, constitutively stimulating hormone synthesis and gland growth. Because the stimulus is receptor agonism rather than opsonization or complement-mediated lysis, the gland is hyperfunctional rather than destroyed. Destructive T cell mediated folliculitis describes Hashimoto thyroiditis, and immune complex deposition is characteristic of Type III diseases such as lupus nephritis.

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

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Written and medically reviewed by the StethoPrep medical team.