Abstract
The most common cause of hyperthyroidism is Graves’ disease, which represents a typical example of an organ-specific autoimmune condition. The exact triggers for the disease remain unknown, but are likely to involve a complex interaction between multiple environmental factors in a genetically predisposed individual. The main feature of the condition is the presence of thyroid-stimulating antibodies, which activate the thyroid- stimulating hormone receptor, resulting in hyperthyroidism. These antibodies may also be involved in the extrathyroidal complications of the disease. The recent generation of thyroid-stimulating antibodies in animal models and the isolation of monoclonal thyroid-stimulating antibodies from a patient with Graves’ disease should allow the detailed study of thyroid-stimulating antibodies–thyroid-stimulating hormone receptor interactions. This will help to shed more light on disease pathogenesis and may offer new treatment strategies in difficult cases, particularly in patients with extrathyroidal complications.