ABSTRACT
Thyroid stimulating hormone (TSH; thyrotropin) is the primary factor for regulating both differentiated function and growth of thyroid follicular epithelial cells (1). The action of TSH is initiated by its binding to TSH receptor (TSHR) on the basolateral site of the thyroid cell plasma membrane, which transduces signals through Gs-cAMP and, to a lesser extent, Gq-phospholipase C cascades. In pathological terms, TSHR involves thyroid autoimmunity and oncogenesis. Thus, TSHR, as well as thyroid peroxidase (TPO) and thyroglobulin (TG), is a target autoantigen in human autoimmune thyroid diseases such as Graves’ disease and Hashimoto’s thyroiditis. Autoantibodies against TSHR stimulate thyroid cells (stimulatory-type autoantibody) or block TSH action (blocking-type autoantibody) (2). Ectopic expression of TSHR may be involved in extrathyroidal manifestations of Graves’ disease such as ophthalmopathy and pretibial myxedema (3). Furthermore, gain-and loss-of-function mutations of the receptor have been found in hyperfunctioning adenoma/congenital nonautoimmune hyperthyroidism and congenital hypothyroidism, respectively (4,5).
