CYCLOHEXIMIDE INHIBITS INTERFERON-GAMMA-INDUCED CLASS-II MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGEN EXPRESSION IN CULTURED RAT-THYROID CELLS

The effects of the agents that are related to intracellular events on interferon-gamma-induced class II major histocompatibility complex antigen expression were studied using the technique of immunocytochemistry. Rat class II major histocompatibility complex antigen (RT1.B) was expressed in 88.3 +/- 3.3% (n = 3) of the functioning rat thyroid cells (FRTL-5) cultured in a medium containing 100 U/ml recombinant rat interferon-gamma (IFN-gamma). Deprivation of bovine TSH had no effect on the expression of RT1.B antigen by IFN-gamma. A23187 (1 nM to 2-mu-M) and/or 10 nM to 10-mu-M phorbol 12-myristate 13-acetate did not induce the expression of RT1.B antigen. IFN-gamma-induced RT1.B expression was not inhibited by either 10 nM to 100-mu-M 1-(5-isoquinolysulfonyl)-2-methylpiperazine or 200 nM to 200 mu-M 8-(N,N-dimethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride. It was also not inhibited by either 5-200-mu-M verapamil or 500 nM to 20-mu-M trifluoperazine. However, 0.01-10-mu-g/ml cycloheximide inhibited IFN-gamma-induced RT1.B antigen expression in a dose-dependent manner. These results suggest that IFN-gamma induces RT1.B antigen expression in FRTL-5 cells via de novo protein synthesis independent of the cAMP system, phosphatidylinositide system, and voltage-dependent calcium channel.