I. Introduction GRAVES' DISEASE is an autoimmune disorder characterized by the presence of stimulatory anti-TSH receptor antibodies which are thought to act via the TSH receptor to increase iodide uptake and cyclic AMP (cAMP), in turn, resulting in T3 and T4 production and secretion (1–7). There have been many clinical articles published summarizing the clinical and laboratory manifestations of Graves' disease (1–7) and excellent reviews of “Autoimmune Thyroid Disease” by Weetman and McGregor (2) and of “Endocrine Ophthalmopathy” by Jacobson and Gorman (8) have been published recently. The purpose of the present review is to discuss in detail the known and suspected immunologic mechanisms which are important in mediating or aggravating Graves' disease and its associated clinical findings. This review will emphasize that our present understanding of normal immune mechanisms of antibody formation, in addition to our comprehension of the perturbations leading to Graves' disease, is inadequate.