THE INFLUENCE OF ANTITHYROID DRUGS AND IODINE ON THYROID CELL MHC CLASS II ANTIGEN EXPRESSION

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Abstract
We have investigated the influence of antithyroid drugs (methimazole and propylthiouracil) and sodium iodide on the expression of major histocompatibility (MHC) class II antigen expression in human and rat thyroid cells. While methimazole and propylthiouracil significantly inhibited lectin-induced MHC class II (HLA-DR) antigen in crude human thyroid monolayer preparations these drugs had no influence on .gamma.-interferon induction of class II antigens in similar cell preparations. Hence, antithyroid drugs probably had a direct effect on thyroid monolayer T cells which are known to effect the lectin induction of MHC class II antigen via T-cell secretion of the cytokine, .gamma.-interferon (IF). Sodium iodide, similarly, had no direct influence on human thyroid cell MHC class II antigen expression induced by .gamma.-IF. However, iodide significantly inhibited the .gamma.-IF-induced expression of MHC class II antigens in a proliferating rat thyroid cell clone derived from FRTL-5 cells (clone 1B-6). In the rat thyroid cell clone this antagonistic action appeared to be exerted via inhibition of TSH-induced proliferation. These data add further support to the multifactorial nature of the profound immunosuppressive influence of antithyroid drugs in autoimmune thyroid disease and experimental thyroiditis. In contrast, iodides may have a major, and often overlooked, influence on thyroid cell proliferation and antigen expression.