期刊
NEUROPHARMACOLOGY
卷 46, 期 5, 页码 734-742出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2003.11.007
关键词
interferon-beta; microglia; antigen presentation; interleukin-12; multiple sclerosis
Interferon-beta (IFNbeta) reduces exacerbations of the relapsing-remitting form of multiple sclerosis (MS), but the exact mechanisms by which it exerts its beneficial effects are unknown. In this study, we examined the effects or IFNbeta on microglial functions, as either antigen presenting cells or effector cells for inflammatory demyelination. IFNbeta significantly suppressed the expression of class II MHC antigen and the co-stimulatory molecule B7-1 in microglia. It also suppressed microglial IL-12 production and differentiation of myelin oligodendrocyte glycoprotein (MOG)-sensitized T cells into the T helper I phenotype. which use microglia as antigen presenting cells. However, IFNbeta significantly and dose-dependently enhanced the production of inflammatory mediators for demyelination, such as TNFalpha, IL-11, 1L-6, and nitric oxide (NO). The upregulation of inflammatory mediators was effectively suppressed with a phosphodiesterase inhibitor. Thus, IFNbeta may exert its suppressive effects in the induction phase, but not in the effector phase of MS. Side effects of IFN treatment may be due to elevation of pro-inflammatory cytokines, and may be reduced by co-treatment with phosphodiesterase inhibitors. (C) 2004 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据