Guillain-Barré syndrome (GBS) is the most common cause of acute paralysis in the United States. Campylobacter jejuni is a common trigger for GBS, igniting autoimmunity as a result of molecular mimicry between C. jejuni lipooligosaccharide (LOS) and host gangliosides. Evidence also suggests an active role for cell-mediated and innate immunity in pathogenesis of GBS. Infection alone is not enough for GBS to develop, infection with the same strain might yield different outcomes in different patients. C. jejuni strains with low to absent molecular mimicry to self-antigens can cause full-blown GBS with positive autoantibodies. A role for T helper 17 and IL-17 in acute phase of GBS is also identified. Currently, no biological treatment is validated for severe, ventilation-dependent patients with GBS, who might not benefit from either IVIG or plasma exchange therapy. Use of biologic agents in treatment-resistant GBS, especially anti-IL-17 agents, such as secukinumab, ixekizumab, and brodalumab, is to be hoped. This review covers up-to-date knowledge on autoimmune mechanisms responsible in different subtypes of GBS: acute inflammatory demyelinating polyneuropathy and acute motor axonal neuropathy; as well as the experimental autoimmune neuritis (EAN), a commonly used animal model of GBS.

中文翻译：

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吉兰-巴雷综合征的自身免疫和细胞因子的重新审查：着眼于治疗选择的病理机制。

Guillain-Barré综合征（GBS）是美国急性麻痹的最常见原因。空肠弯曲杆菌是GBS的常见诱因，由于空肠弯曲杆菌脂寡糖（LOS）和宿主神经节苷脂之间的分子模拟，可引发自身免疫。证据还表明，在GBS的发病机理中，细胞介导的先天免疫具有积极作用。单纯的感染不足以促进GBS的发展，同一菌株的感染可能在不同患者中产生不同的结果。空肠弯曲菌对自身抗原的分子模仿性低至缺失的菌株可导致具​​有阳性自身抗体的成熟GBS。还确定了T辅助剂17和IL-17在GBS急性期中的作用。目前，尚没有针对严重，通气依赖的GBS患者（未从IVIG或血浆置换治疗中获益）进行任何生物治疗的验证。希望在抗药性GBS中使用生物制剂，尤其是抗IL-17制剂，例如secukinumab，ixekizumab和brodalumab。这篇综述涵盖了有关GBS的不同亚型的自身免疫机制的最新知识：急性炎症性脱髓鞘性多发性神经病和急性运动性轴索神经病；以及实验性自身免疫性神经炎（EAN），即GBS的常用动物模型。