Iii. Clinical Course of Ted

GD is an autoimmune disease where circulating antibodies cause hyperthyroidism and lead to thyrotoxicosis. These antibodies, originally referred to as long-acting thyroid stimulators, are directed against the thyrotropin receptor (TSHR). They mimic the agonist activity of TSH but are not subject to the normal feedback in the anterior pituitary. GD is approximately 7 to 10 fold more frequent in women, and typically occurs between 20 and 50 years of age. Clinical manifestations of GD encompass thyroid enlargement and thyrotoxicosis, inflammation and remodeling of the orbit, and rarely the skin. The orbital disease is collectively known as thyroid-associated ophthalmopathy aka thyroid eye disease (TED). It is unclear why anatomically unrelated tissues undergo coordinate and selective immune infiltration and remodeling. Furthermore, the mechanistic basis for the self-limited course of the orbital disease is unclear, but identifying these underlying factors could provide insights necessary for the development of effective therapies. This article summarizes our current understanding of TED, focusing on the fundamental aspects of its molecular pathogenesis. In it we identify attractive potential targets for interrupting the disease.