ABSTRACT
What we now understand to be autoimmune hyperthyroidism was initially observed by Caleb Parry in 1825, but first described in print by Robert Graves in 1835 (1). These physicians recognized the combination of goiter and prominent staring eyes in patients with heart failure. However, the concept of Graves’ disease as a unique organ-specific autoimmune disease was not introduced until 1956, when Adams and Purves discovered TSH receptor autoantibodies [then termed long-acting thyroid stimulator or “LATS” (2)]. Indeed, the discovery of autoantibodies to thyroglobulin in patients with autoimmune thyroiditis as well as patients with Graves’ disease (3) captured the imagination of thyroidologists and immunologists and demonstrated that these thyroid diseases were indeed the first confirmed human autoimmune diseases. Since those early days, there has been progress in the understanding of human thyroid autoimmunity, but Graves’ disease remains an enigma; a uniquely human disease. In addition, the accessibility of the thyroid gland has caused both autoimmune hyperthyroidism and hypothyroidism to remain models for understanding self tolerance and its breakdown.
