Abstract
Graves’ disease is an autoimmune disorder of the thyroid (Adams, 1981) characterized by a goiter and hyperthyroidism. The concept that the signs and symptoms of Graves’ disease reflected the action of circulating antibodies to the TSH receptor evolved because thyroid stimulating antibodies (TSAbs) increased adenylate cyclase activity as did TSH (McKenzie and Zakarija, 1977; Zakarija and McKenzie, 1980; Adams, 1981; Kasagi, et al., 1982) and because IgG preparations from Graves’ patients could inhibit TSH binding to thyroid membrane preparations (TBIAb activity) (Smith and Hall, 1974; Hanley et al. 1974; Mehdi and Nussey, 1975). It was argued the two activities were exhibited by the same antibody. Unfortunately the concept ran into several problems. Thus, in most studies, assays measuring thyroid stimulating antibodies (TSAbs) and thyrotropin binding inhibiting antibodies (TBIAbs) did not correlate in a significant number of patients. (Ozawa et al, 1979; Sugenoya et al, 1979; Pinchera et al, 1980; Zakarija and McKenzie, 1980; Macchia et al, 1981). Further several studies indicated that the growth stimulating activity of Graves’ IgG preparations did not correlate with the thyroid stimulating activity in all cases, (Doniach et al, 1980; Drexhage et al, 1980, 1981; Valente et al, 1983).
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References
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Chan, J. et al. (1987). Nature of Thyroid Autoantigens: The TSH Receptor. In: Pinchera, A., Ingbar, S.H., McKenzie, J.M., Fenzi, G.F. (eds) Thyroid Autoimmunity. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0945-1_2
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