In Graves disease, autoantibodies bind the TSH receptor on thyroid follicular cells and stimulate hormone synthesis and gland growth rather than causing cell lysis. According to the Gell and Coombs framework, this reaction is best classified as:

• A Type I hypersensitivity mediated by IgE on mast cells
• B Type III hypersensitivity driven by circulating immune complexes
• C Type II hypersensitivity, a variant in which antibody causes functional stimulation instead of cell destruction ✓
• D Type IV hypersensitivity mediated by CD8 positive cytotoxic T cells

Explanation

Graves disease is classified as type II (antibody mediated) hypersensitivity because IgG antibodies bind a fixed cell surface antigen, the TSH receptor. Unlike classic type II reactions that destroy cells via complement or ADCC, here the antibody is agonistic and stimulates the receptor, historically termed long acting thyroid stimulator activity. Robbins explicitly cites Graves disease as the example of this stimulatory subtype of type II disease, distinguishing it from immune complex injury of type III and T cell mediated type IV mechanisms.

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.