Loughlin, A. J.; Woodroofe, M. N. and Cuzner, M. L.
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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-beta 1 (TGF-beta 1) 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-gamma (IFN-gamma). The effect of IL-4 or TGF-beta 1 in combination with IFN-gamma, added either sequentially or simultaneously, has been investigated. TGF-beta 1 down-regulates IFN-gamma-induced effects in both microglia and macrophages when present before or during the activation stage. In combination, IL-4 and IFN-gamma 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-gamma-induced activation of microglia and macrophages.
|Item Type:||Journal Article|
|Copyright Holders:||1993 Blackwell Publishing|
|Project Funding Details:||
|Academic Unit/Department:||Faculty of Science, Technology, Engineering and Mathematics (STEM) > Life, Health and Chemical Sciences
Faculty of Science, Technology, Engineering and Mathematics (STEM)
|Interdisciplinary Research Centre:||Biomedical Research Network (BRN)|
|Depositing User:||Jane Loughlin|
|Date Deposited:||20 Apr 2011 09:50|
|Last Modified:||04 Oct 2016 10:57|
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