The pathophysiology of autoimmune thyroid disease.

Evidence is presented favouring a partial antigen-specific defect in suppressor T lymphocytes as the basis for autoimmune thyroid disease (AITD). This in turn may well be due to an HLA-related gene abnormality in specific antigen presentation to T lymphocytes, resulting in inadequate induction (activation) of antigen-specific suppressor T lymphocytes. The additive effect of environmental factors adversely affecting overall suppressor T cell function may serve to precipitate AITD. The consequent activation of specific helper T lymphocytes leads to cytokine and thyroid autoantibody production, and the combined effects of cytokines, thyroid antibodies and cellular components on thyrocytes completes the pathological picture. The pathophysiology of AITD is further affected by the actions of the thyrocyte in communicating with the immune system (thyrocyte-immunocyte signalling), through thyrocyte HLA-DR expression, thyroid antigen expression, and the effect of thyroid hormone itself on the immune system. Interference of these signals by therapeutic modalities may lead to amelioration of the immune process, or even remissions.