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格林-巴利综合征的感染性和非感染性触发因素。

Infectious and noninfectious triggers in Guillain-Barré syndrome.

机构信息

Department of Medicine, National University Hospital, 1E Kent Ridge Road, Singapore.

出版信息

Expert Rev Clin Immunol. 2013 Jul;9(7):627-39. doi: 10.1586/1744666X.2013.811119.

DOI:10.1586/1744666X.2013.811119
PMID:23899233
Abstract

Guillain-Barré syndrome (GBS) is the commonest cause of acquired flaccid paralysis in the world and regarded by many as the prototype for postinfectious autoimmunity. Here the authors consider both infectious and noninfectious triggers of GBS and determine where possible what immunological mechanisms may account for this association. In approximately two-thirds of cases, an infectious trigger is reported in the weeks that lead up to disease onset, indicating that the host's response to infection must play an important role in disease pathogenesis. The most frequently identified bacteria, Campylobacter jejuni, through a process known as molecular mimicry, has been shown to induce cross-reactive anti-ganglioside antibodies, which can lead to the development of axonal-type GBS in some patients. Whether this paradigm can be extended to other infectious organisms or vaccines remains an important area of research and has public health implications. GBS has also been reported rarely in patients with underlying systemic diseases and immunocompromised states and although the exact mechanism is yet to be established, increased susceptibility to known infectious triggers should be considered most likely.

摘要

格林-巴利综合征(GBS)是世界上最常见的获得性弛缓性瘫痪的病因,许多人认为它是感染后自身免疫的典型代表。在这里,作者同时考虑了 GBS 的感染性和非感染性触发因素,并尽可能确定哪些免疫机制可能与之相关。大约三分之二的病例报告称,在疾病发作前的几周内存在感染性触发因素,这表明宿主对感染的反应在疾病发病机制中必须发挥重要作用。最常被识别的细菌空肠弯曲菌通过一种称为分子模拟的过程,已被证明能诱导交叉反应性抗神经节苷脂抗体,这可能导致一些患者发生轴索性 GBS。这一范式是否可以扩展到其他感染性生物体或疫苗仍然是一个重要的研究领域,具有公共卫生意义。GBS 也很少在患有基础系统性疾病和免疫功能低下的患者中报告,尽管确切的机制尚未确定,但应考虑增加对已知感染性触发因素的易感性。

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