Thyroid-stimulating antibody

In Graves disease, hyperthyroidism results from the action of thyroid-stimulating antibodies (TSAb) directed against the thyrotropin receptor on the surface of the thyroid cell. These immunoglobulin G antibodies bind to the receptor and activate the enzyme adenylate cyclase in the same manner as TSH. 

Q6 Graves disease is an autoimmune disease caused by the presence of thyroid stimulating antibodies which attack the TSH receptors in the thyroid gland, preventing the TSH from binding to its receptors. 

Evaluation and validation of a microassay for cAMP measurement on detecting thyroid stimulating antibodies using FRTL-5 cells. CHn Chem 1995 41 540. 

Massart C, Hody B, Mouchel L, Edan G, Nicol M. Assays for thyrotropin-receptor binding and thyroid-stimulating antibodies in sera from patients with Graves disease. CUn Chem 1986 32 1332-5,... 

Thyrotoxicosis is most commonly caused by Graves disease, which is an autoimmune disorder in which thyroid-stimulating antibody (TSAb) directed against the thyrotropin receptor elicits the same biologic response as thyroid-stimulating hormone (TSH). 

TR 82, TR/31, TRal thyroid hormone receptors TRH thyrotropin-releasing hormone TSAb thyroid-stimulating antibody TSH thyroid-stimulating hormone... 

Etiology Thyroid-stimulating antibodies bind to TSH receptors, causing release of thyroxin (current theory). 

To summarize the results of the experiments described above, it appears that 1) in response to injections of thyroid gland homogenate an antibody was formed in rabbits which acted as a thyroid stimulator when injected into mice 2) the thyroid-stimulating antibody affected the host rabbit s own thyroid function so that it became "non-suppressible" by the injection of thyroxine. 

There is no evidence that the rabbits with thyroid-stimulating antibody in their blood were hyperthyroid and, indeed, the normal release rate of thyroid radioiodine probably indicates they were not. It would therefore be reasonable to question why they were not hyperthyroid or, in a similar vein, if they are likely to become so. The following points may be relevant to these considerations. 

Adams DD, Kennedy TH, Stewart JC, Utiger RD, Vidor GI. 1975. Hyperthyroidism in Tasmania following iodide supplementation Measurements of thyroid stimulating antibodies and thyrotropin. J Clin Endocrinol Metab 41, 221-228. 

Laurent, E., Van Sande, J., Ludgate, M., Corvilain, B., Rocmans, P., Dumont, J.E., Mockel, J., 1991, Unlike thyrotropin, thyroid-stimulating antibodies do not activate phosphohpase C in human thyroid shces, J. Clin. Invest. 87 1. 

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