MODULATION OF INTERFERON-GAMMA-INDUCED MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II AND FC-RECEPTOR EXPRESSION ON ISOLATED MICROGLIA BY TRANSFORMING GROWTH-FACTOR-BETA-1, INTERLEUKIN-4, NORADRENALINE AND GLUCOCORTICOIDS

Interleukin-4 (IL-4) enhances Fc receptor (FcR) expression on isolated rat brain microglia and peritoneal macrophages but has little effect on major histocompatibility complex (MHC) class II antigen expression. In contrast transforming growth factor-beta1 (TGF-beta1) causes a red uction in expression of MHC class II on macrophages and of FcR on both cell types. Both microglia and peritoneal macrophages demonstrate enh anced expression of FcR and MHC class II on treatment with interferon- gamma (IFN-gamma). The effect of IL-4 or TGF-beta1 in combination with IFN-gamma, added either sequentially or simultaneously, has been inve stigated. TGF-beta1 down-regulates IFN-gamma-induced effects in both m icroglia and macrophages when present before or during the activation stage. In combination, IL-4 and IFN-gamma can be additive or antagonis tic, depending on their concentrations and the sequence in which cells are exposed to the cytokines. Non-cytokine mediators present during s timulation, such as noradrenaline, dexamethasone and corticosterone, a re also potent inhibitors of IFN-gamma-induced activation of microglia and macrophages.