The Immunoregulatory Disturbance in Autoimmune Thyroid Disease

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Abstract
There is now considerable evidence for a genetically induced antigen-specific defect in suppressor T lymphocytes as the basis for AITD, derived from several laboratories and via different types of experimental techniques. In addition, there is now evidence for additive effects on reducing generalized suppressor T lymphocyte numbers and/or function by environmental factors as well as hyperthyroidism itself, and these effects would be superimposed upon the organ-specific defect. Such effects on generalized suppressor T lymphocyte numbers may act as precipitating and self-perpetuating factors, in Graves' disease at least. Presentation of the antigen by the thyroid cell via HLA-DR expression on its membrane does occur as a result of interferon gamma production by T lymphocytes. This in turn appears to be secondary to the initial specific immune assault and is not a primary inductive step. However, it may be important as an amplifying intermediate factor but cannot perpetuate the process in the absence of the underlying immune disorder. There is, however, no evidence for an underlying antigenic abnormality or stimulus in human autoimmune thyroid disease, and the initiating event would appear to be due to perturbation of the generalized immune system superimposed on the organ-specific abnormality. Variations in the serological and clinical expression of AITD would appear to depend on the severity of the original organ-specific disturbance in suppressor T lymphocyte function, plus the added factor of environmental influences playing upon generalized suppressor T lymphocyte function and numbers. Remissions in Graves' disease brought about by antithyroid drugs may well be via their effect on modulating the thyroid cell activity; this will then reduce thyrocyte-immunocyte signalling, allowing remission to occur in those patients with a partial organ-specific defect in suppressor T lymphocytes.

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