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[多发性硬化症的发病机制与治疗。细胞因子的作用]

[Pathogenesis and therapy of multiple sclerosis. The role of cytokines].

作者信息

Weber F, Rieckmann P

机构信息

Neurologische Universitätsklinik Göttingen.

出版信息

Nervenarzt. 1995 Feb;66(2):150-5.

PMID:7715757
Abstract

Multiple sclerosis (MS) is probably caused by multiple factors, but there is evidence that an autoimmunological process is relevant for the pathogenesis. Cytokines can operate in different ways in MS and the animal model "experimental allergic encephalomyelitis (EAE). "Interferon gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), TNF-beta, interleukin-1 (IL-1) and IL-2 are important inflammation mediators within the MS plaque, whereas IFN-alpha, IFN-beta, transforming-growth-factor-beta (TGF-beta) and IL-10 exert mainly immunosuppressive functions. Application of these anti-inflammatory cytokines and the selective block of pro-inflammatory cytokines are promising new therapeutic strategies with fewer side effects than the commonly used cytostatic drugs.

摘要

多发性硬化症(MS)可能由多种因素引起,但有证据表明自身免疫过程与发病机制相关。细胞因子在MS和动物模型“实验性变应性脑脊髓炎(EAE)”中可通过不同方式发挥作用。γ干扰素(IFN-γ)、肿瘤坏死因子-α(TNF-α)、TNF-β、白细胞介素-1(IL-1)和IL-2是MS斑块内重要的炎症介质,而α干扰素、β干扰素、转化生长因子-β(TGF-β)和IL-10主要发挥免疫抑制功能。应用这些抗炎细胞因子以及选择性阻断促炎细胞因子是有前景的新治疗策略,其副作用比常用的细胞毒性药物更少。

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1
[Pathogenesis and therapy of multiple sclerosis. The role of cytokines].[多发性硬化症的发病机制与治疗。细胞因子的作用]
Nervenarzt. 1995 Feb;66(2):150-5.
2
Defective production of anti-inflammatory cytokine, TGF-beta by T cell lines of patients with active multiple sclerosis.活动性多发性硬化症患者T细胞系抗炎细胞因子转化生长因子-β(TGF-β)产生缺陷。
J Immunol. 1994 Jun 15;152(12):6003-10.
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The phosphodiesterase i.v. inhibitor rolipram in vitro reduces the numbers of MBP-reactive IFN-gamma and TNF-alpha mRNA expressing blood mononuclear cells in patients with multiple sclerosis.磷酸二酯酶静脉内抑制剂咯利普兰在体外可减少多发性硬化症患者中表达髓鞘碱性蛋白反应性γ干扰素和肿瘤坏死因子-α信使核糖核酸的血液单核细胞数量。
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Pro- versus anti-inflammatory cytokines: myth or reality.促炎细胞因子与抗炎细胞因子:神话还是现实。
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Increased transforming growth factor-beta, interleukin-4, and interferon-gamma in multiple sclerosis.多发性硬化症中转化生长因子-β、白细胞介素-4和干扰素-γ水平升高。
Ann Neurol. 1994 Sep;36(3):379-86. doi: 10.1002/ana.410360309.
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[T-cell interferon-gamma, tumor necrosis factor-alpha and interleukin-6 receptor binding in patients with multiple sclerosis. Effects of interferon-beta-1b treatment].[多发性硬化症患者的T细胞干扰素-γ、肿瘤坏死因子-α和白细胞介素-6受体结合。β-1b干扰素治疗的效果]
Rev Neurol. 1999;29(10):893-9.
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Interferon-beta enhances monocyte and dendritic cell expression of B7-H1 (PD-L1), a strong inhibitor of autologous T-cell activation: relevance for the immune modulatory effect in multiple sclerosis.β干扰素增强B7-H1(程序性死亡配体1)在单核细胞和树突状细胞中的表达,B7-H1是自体T细胞活化的强效抑制剂:对多发性硬化症免疫调节作用的相关性。
J Neuroimmunol. 2004 Oct;155(1-2):172-82. doi: 10.1016/j.jneuroim.2004.06.013.
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TGF-beta as a promising option in the treatment of multiple sclerosis.转化生长因子-β作为治疗多发性硬化症的一种有前景的选择。
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Short-term treatment of relapsing remitting multiple sclerosis patients with interferon (IFN)-beta1B transiently increases the blood levels of interleukin (IL)-6, IL-10 and IFN-gamma without significantly modifying those of IL-1beta, IL-2, IL-4 and tumour necrosis factor-alpha.用干扰素(IFN)-β1B对复发缓解型多发性硬化症患者进行短期治疗,可使白细胞介素(IL)-6、IL-10和IFN-γ的血液水平短暂升高,而不会显著改变IL-1β、IL-2、IL-4和肿瘤坏死因子-α的水平。
Cytokine. 2000 Jun;12(6):682-7. doi: 10.1006/cyto.1999.0616.
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Regulatory effects of IFN-beta on production of osteopontin and IL-17 by CD4+ T Cells in MS.干扰素-β对多发性硬化症中CD4 + T细胞产生骨桥蛋白和白细胞介素-17的调节作用。
Eur J Immunol. 2009 Sep;39(9):2525-36. doi: 10.1002/eji.200838879.

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