THE INFLUENCE OF TRIIODOTHYRONINE, THYROXINE, THYROTROPIN, AND METHIMAZOLE ON THYROID-CELL MHC CLASS-II ANTIGEN EXPRESSION

We have studied the influence of triiodothyronine (T-3), thyroxine (T- 4), thyrotropin (TSH), and methimazole (MMI) on the expression of majo r histocompatibility (MHC) Class II antigen expression in human thyroi d cells, T-3, T-4, TSH, and MMI in various combinations were added tog ether with interferon-gamma (IFN-gamma) to human thyrocytes or to cult ured FRTL-B cells, Neither T-3 nor T-4, alone, caused inhibition of th e IFN-gamma stimulation of thyrocyte HLA-DR expression. Moreover, the combination of both drugs at various concentrations did not inhibit th is expression except only in low ranges (T-3 at 0.3 nmol/liter and T-4 at 12.9 nmol/liter). MMI only at a concentration of 3.0 mmol/liter ca used significant inhibition of IFN-gamma-induced HLA-DR expression, Ho wever, the addition of T-3 (range, 0.3-9.2 nmol/liter) or T-4 (12.9-12 9.0 nmol/liter) prevented the MMI-induced inhibition. This phenomenon may be explained by the action of MMI on inhibiting the synthesis of T -3 and T-4. At a concentration of 100 mu U/ml, TSH enhanced IFN-gamma- induced HLA-DR expression. It is possible that TSH induced the express ion of large numbers of IFN-gamma receptors, thereby enhancing the pro duction of HLA-DR in response to IFN-gamma. Our studies suggest that M MI does not alter thyrocyte HLA-DR expression in vitro, especially whe n combined with T-3 or T-4; however, MMI may still induce or perpetuat e immune effects in vivo secondary to its influence on thyroid hormone production or thyroid antigen presentation. (C) 1995 Academic Press, Inc.