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一种新的细胞酶联免疫吸附测定法表明,在多发性硬化症中,β干扰素可抑制γ干扰素。

A new cell enzyme-linked immunosorbent assay demonstrates gamma interferon suppression by beta interferon in multiple sclerosis.

作者信息

Bakhiet M, Ozenci V, Withagen C, Mustafa M, Fredrikson S, Link H

机构信息

Divisions of Infectious Diseases and Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.

出版信息

Clin Diagn Lab Immunol. 1999 May;6(3):415-9. doi: 10.1128/CDLI.6.3.415-419.1999.

DOI:10.1128/CDLI.6.3.415-419.1999
PMID:10225846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC103733/
Abstract

Multiple sclerosis (MS) is a demyelinating disorder of the central nervous system of unknown etiology. Immune mechanisms involving the proinflammatory cytokine gamma interferon (IFN-gamma) are believed to play an important role in the pathogenesis of MS. IFN-beta-1b has been introduced as a treatment for MS and was found to reduce the number and severity of clinical exacerbations. To examine the influence of IFN-beta-1b on myelin basic protein (MBP)-specific and phytohemagglutinin-induced IFN-gamma production, we developed a cell-released capturing enzyme-linked immunosorbent assay (CRC-ELISA), which rapidly measures spontaneous and antigen- or mitogen-induced cellular IFN-gamma production. CRC-ELISA documented a significant MBP-specific T-cell response in the blood of untreated MS patients, as assessed by IFN-gamma production. This response was suppressed in MS patients treated with IFN-beta-1b. The present work confirms in vivo the in vitro suppressive effects of IFN-beta-1b on IFN-gamma production in MS. Moreover, it provides a powerful new technique for detection of cytokines.

摘要

多发性硬化症(MS)是一种病因不明的中枢神经系统脱髓鞘疾病。涉及促炎细胞因子γ干扰素(IFN-γ)的免疫机制被认为在MS的发病机制中起重要作用。IFN-β-1b已被引入作为MS的一种治疗方法,并且发现它能减少临床病情加重的次数和严重程度。为了研究IFN-β-1b对髓鞘碱性蛋白(MBP)特异性和植物血凝素诱导的IFN-γ产生的影响,我们开发了一种细胞释放捕获酶联免疫吸附测定法(CRC-ELISA),该方法可快速测量自发的以及抗原或丝裂原诱导的细胞IFN-γ产生。通过IFN-γ产生评估,CRC-ELISA记录了未经治疗的MS患者血液中显著的MBP特异性T细胞反应。在用IFN-β-1b治疗的MS患者中,这种反应受到抑制。目前的研究在体内证实了IFN-β-1b对MS中IFN-γ产生的体外抑制作用。此外,它为细胞因子的检测提供了一种强大的新技术。

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本文引用的文献

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Interferon-beta 1b treatment decreases tumor necrosis factor-alpha and increases interleukin-6 production in multiple sclerosis.干扰素-β1b治疗可降低多发性硬化症患者的肿瘤坏死因子-α水平并增加白细胞介素-6的产生。
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Dissociation between cytokine mRNA expression and protein production in shigellosis.志贺氏菌病中细胞因子mRNA表达与蛋白质产生之间的解离。
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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。
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The astrocyte mitogen, tumor necrosis factor-alpha, inhibits the proliferative effect of more potent adult human astrocyte mitogens, gamma-interferon and activated T-lymphocyte supernatants.
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