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The Role of Autoimmunity in Hypoendocrine and Hyperendocrine Function: With Special Emphasis on Autoimmune Thyroid Disease

[+] Article, Author, and Disclosure Information

Grant support: work cited from the author's laboratory has been supported by grants from the Medical Research Council of Canada (MT859).

This paper was presented as a "State of the Art" address at the 58th annual meeting of The Endocrine Society, 23-25 June 1976, San Francisco, California.

▸Requests for reprints should be addressed to Robert Volpé, M.D.; Room 112D, Jones Bldg., The Wellesley Hospital, 160 Wellesley St. E.; Toronto, ON M4Y 1J3, Canada.

Toronto, Canada

Ann Intern Med. 1977;87(1):86-99. doi:10.7326/0003-4819-87-1-86
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There is considerable evidence to suggest that the organspecific autoimmune endocrinopathies are primary disorders of the lymphoid system. Although proof is not complete, the basic genetic defect in each condition may be one of immune surveillance, that is, a defect in suppressor "T" lymphocytes. Combinations of two or more of these conditions may be due to the concurrence of two or more specific defects in immune control, as well as the random appearance of the appropriate self-directed "forbidden" clones of lymphocytes. In this concept, there is no need for antigenic alteration (only antigenic availability) to initiate these disorders. Both cell-mediated and humoral immunity seem essential, with roles for immune complexes and "killer" cells as well. Antireceptor antibodies are of particular interest in Graves' disease, where they are stimulatory: other antireceptor antibodies have been found that are blocking antibodies, and others may merely bind without either stimulating or blocking.





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