학술논문
Modulation of interferon-γ-induced major histocompatibility complex class II and Fc receptor expression on isolated microglia by transforming growth factor-β1, interleukin-4, noradrenaline and glucocorticoids.
Document Type
Article
Author
Source
Subject
*MAJOR histocompatibility complex
*INTERFERONS
*MICROGLIA
*TRANSFORMING growth factors-beta
*INTERLEUKIN-4
*NORADRENALINE
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Language
ISSN
0019-2805
Abstract
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-β1 (TGF-β1) causes a reduction in expression of MHC class II on macrophages and of FcR on both cell types. Both microglia and peritoneal macrophages demonstrate enhanced expression of FcR and MHC class II on treatment with interferon-γ (IFN-γ). The effect of IL-4 or TGF-β1 in combination with IFN-γ, added either sequentially or simultaneously, has been investigated. TGF-β1 down-regulates IFN-γ-induced effects in both microglia and macrophages when present before or during the activation stage. In combination, IL-4 and IFN-γ can be additive or antagonistic, depending on their concentrations and the sequence in which cells are exposed to the cytokines. Non-cytokine mediators present during stimulation, such as noradrenaline, dexamethasone and corticosterone, are also potent inhibitors of IFN-γ-induced activation of microglia and macrophages. [ABSTRACT FROM AUTHOR]