Autoantibodies and Neuropathic Pain

J. Dawes, D. Bennett
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引用次数: 4

Abstract

A number of clinical studies indicated an association between autoantibodies and neuropathic pain. This is supported by the observation that immunotherapies that reduce antibody levels alleviate pain in patients and suggests that autoantibodies are not a byproduct of pathology but instead important drivers of neuropathic pain. These autoantibodies can target both neuronal and nonneuronal antigens within the sensory nervous system. Possible pathogenic mechanisms include nerve damage and inflammation as well as disruption of ion channel function. Whether autoantibodies are truly causal to neuropathic pain and exactly what their prevalence is in such pain conditions are important questions that are being addressed with the use of passive transfer in preclinical models and the screening of patient sera. Such studies support the idea that autoantibodies are a mechanism to cause neuropathic pain and provide insight into the molecular components regulating pain sensitivity in a pathological setting. Therefore, this work not only will be applicable to the treatment of patients with autoantibody-mediated pain, but also will facilitate the development of therapies to treat neuropathic pain in the more general context.
自身抗体与神经性疼痛
许多临床研究表明,自身抗体与神经性疼痛之间存在关联。观察结果支持了这一点,即降低抗体水平的免疫疗法减轻了患者的疼痛,并表明自身抗体不是病理的副产物,而是神经性疼痛的重要驱动因素。这些自身抗体可以靶向感觉神经系统中的神经元和非神经元抗原。可能的致病机制包括神经损伤和炎症以及离子通道功能的破坏。自身抗体是否真的是神经性疼痛的原因,以及它们在这种疼痛条件下的确切患病率是什么,这些都是重要的问题,正在通过在临床前模型和患者血清筛选中使用被动转移来解决。这些研究支持了自身抗体是引起神经性疼痛的机制的观点,并提供了在病理环境中调节疼痛敏感性的分子成分的见解。因此,这项工作不仅将适用于治疗自身抗体介导的疼痛患者,而且将促进在更普遍的情况下治疗神经性疼痛的疗法的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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