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干扰素α与神经肌肉疾病

Interferon alpha and neuromuscular disorders.

作者信息

Stübgen Joerg-Patrick

机构信息

Department of Neurology and Neuroscience, Weill Medical College of Cornell University/New York Presbyterian Hospital, USA.

出版信息

J Neuroimmunol. 2009 Feb 15;207(1-2):3-17. doi: 10.1016/j.jneuroim.2008.12.008. Epub 2009 Jan 25.

Abstract

Interferon-alpha (IFNalpha) is a potent extracellular protein mediator of host defense and homeostasis. IFNalpha has well-established direct antiviral, antiproliferative and immunomodulatory properties. The worldwide, increasing and long-term use of IFNalpha, particularly for the treatment of chronic hepatitis C virus infection, has drawn attention to the development or exacerbation of numerous autoimmune phenomena, including a variety of neuropathy syndromes, neuromuscular junction disorders and myopathies. Management entailed withdrawal of IFNalpha therapy with supportive, immunomodulatory, and symptomatic treatment as clinically indicated. The mechanisms of IFNalpha-induced autoimmunity are incompletely understood, and likely vary depending on the inherent differences in the pathogenesis of the immune disorder on a background of patient genetic susceptibility. In addition, there is preliminary evidence from case reports and open-label studies that the immunomodulatory effects of IFNalpha may have potential as a treatment option for a spectrum of immune-mediated neuromuscular diseases, but further studies are needed.

摘要

干扰素-α(IFNα)是宿主防御和内环境稳定的一种强效细胞外蛋白介质。IFNα具有公认的直接抗病毒、抗增殖和免疫调节特性。在全球范围内,IFNα的使用日益增加且长期应用,尤其是用于治疗慢性丙型肝炎病毒感染,这已引起人们对多种自身免疫现象的发生或加重的关注,这些现象包括各种神经病变综合征、神经肌肉接头疾病和肌病。处理措施包括停用IFNα治疗,并根据临床指征进行支持性、免疫调节和对症治疗。IFNα诱导自身免疫的机制尚未完全明确,并且可能因患者遗传易感性背景下免疫疾病发病机制的固有差异而有所不同。此外,病例报告和开放标签研究的初步证据表明,IFNα的免疫调节作用可能有潜力作为一系列免疫介导的神经肌肉疾病的一种治疗选择,但还需要进一步研究。

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