P cell stimulating factor and glucocorticoids oppose the action of interferon-gamma in inducing Ia antigens on T-dependent mast cells (P cells).

The expression of Ia antigens of cultured lines of T-dependent mast cells (TDMC) or persisting (P) cells was modulated by three hormones: interferon-gamma (IFN-gamma), P cell-stimulating factor (PSF), and glucocorticoids. The induction of Ia antigens by cloned IFN-gamma was inhibited by a homogeneous preparation of PSF, the T cell-derived factor that TDMC require for their in vitro growth. This inhibitory effect of PSF was dose-dependent and could not be overcome by increasing the levels of IFN-gamma. Other cytokines such as granulocyte/macrophage colony-stimulating factor, T cell growth factor, and L cell-derived macrophage colony-stimulating factor had no inhibitory effect. Thus, two different T cell lymphokines, PSF and IFN-gamma, have opposing effects on the expression of Ia antigens on TDMC. Glucocorticoids (hydrocortisone, corticosterone, dexamethasone, prednisolone, and fludrocortisone) antagonized the induction of Ia antigens by IFN-gamma, whereas sex steroids (progesterone, estradiol, and testosterone) and a mineralocorticoid (aldosterone) did not. The inhibitory effect of glucocorticoids could not be overcome by increasing concentrations of IFN-gamma, but was significantly inhibited by progesterone (10(-6) M), indicating the likely involvement of typical glucocorticoid receptors. In contrast to their effectiveness on macrophages, prostaglandin E2 and dibutyryl cyclic AMP only slightly inhibited the induction of Ia antigens on TDMC by IFN-gamma, whereas endotoxin (1 to 60 micrograms/ml) had no effect.