1. Proposed pathogenesis of Graves disease
Proposed pathogenesis of Graves disease. A defect in suppressor T lymphocytes (Ts) allows helper T lymphocytes (TH) to stimulate B lymphocytes (B) to synthesize thyroid autoantibodies. The thyroid receptor–stimulating antibody (TSH-R [stim] Ab) is the driving force for thyrotoxicosis. Inflammation of the orbital muscles may be due to sensitization of cytotoxic T lymphocytes (Tc), or killer cells, to orbital antigens linked to an antigen in the thyroid. What triggers this immunologic cascade is not known. Ag, antigen; P Ab, peroxidase or microsomal antibody; Tg Ab, thyroglobulin antibody. (Redrawn, with permission, from Gardner DG et al, eds. Greenspan’s Basic and Clinical Endocrinology, 9th ed. McGraw-Hill, 2011.)
Source: Thyroid Disease, Pathophysiology of Disease: An Introduction to Clinical Medicine, 7e
Citation: Hammer GD, McPhee SJ. Pathophysiology of Disease: An Introduction to Clinical Medicine, 7e; 2013 Available at: Accessed: November 06, 2017
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