Abstract
It has been hypothesized over many years that the autoimmune endocrine diseases are each due to antigen-specific defects in suppressor (regulatory) T lymphocyte function. There is now increasing evidence in studies of autoimmune thyroid disease and insulin-dependent diabetes mellitus that suppressor cells are activated by irrelevant antigens but respond inadequately to specific relevant antigens. These inadequate responses are insufficient in themselves to precipitate the autoimmune disease; further insults from the environment increase the deficiencies in regulatory cell activity, adding to the genetically induced dysfunction, i.e., specific defects in antigen presentation. Diagnostic procedures for autoimmune endocrine diseases include tests of target cell function and the detection of various antibodies, which are becoming increasingly useful in prediction, diagnosis, and management of these diseases.
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