Regulation of major histocompatibility complex class II antigen expression by the FRTL-5 rat thyroid cell line.

Abstract

We have used the continuously growing FRTL-5 rat thyroid cell line to examine the regulation of major histocompatibility complex (MHC) class II (or Ia) antigen expression. Of the various stimuli investigated, only the supernatant from activated T cells or recombinant gamma-interferon induced Ia expression. All Ia-inducing activity was removed from the T cell supernatant by acid dialysis, suggesting that gamma-interferon is the single critical mediator for class II antigen expression. Its action was not TSH dependent but expression of class II antigens increased from the G0-G1 to the S and G2 phases of the cell cycle, so that TSH enhanced Ia expression by its action on cell division. Other agents including lectins, hormones, epidermal growth factor, a calcium ionophore and a phorbol ester did not induce Ia expression. Substances known to inhibit murine macrophage Ia expression (cortisol, prostaglandin E2 and 5-hydroxytryptamine) had no effect on FRTL-5 Ia expression. The use of this thyroid cell line has permitted direct examination of modulators in the absence of any possible effects from contaminating non-thyroid cells present in primary cultures and the results suggest that, of the agents tested, only gamma-interferon has significance in the context of Ia antigen expression by the thyroid.