Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogota, Colombia.
Division of Rheumatology, Allergy and Clinical Immunology, University of California Davis, School of Medicine, Davis, USA, CA.
Cell Mol Immunol. 2018 Jun;15(6):547-562. doi: 10.1038/cmi.2017.142. Epub 2018 Jan 29.
Guillain-Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.
格林-巴利综合征（GBS）和横贯性脊髓炎（TM）均为具有重要临床意义的免疫介导性多发性神经病。两者都被认为具有遗传易感性，但迄今为止，尚未明确界定特定的遗传风险位点。两者均被认为是自身免疫性疾病，但病因仍不清楚。两者都可能通过分子模拟而引发，特别是来自感染因子和疫苗，但宿主因素和共存的宿主反应显然会调节疾病易感性和自然病程。GBS 是一种急性炎症性免疫介导性多发神经根神经病，其特征为刺痛、进行性无力、自主神经功能障碍和疼痛。免疫损伤主要发生在急性炎症性脱髓鞘性多发性神经病中的髓鞘和相关雪旺细胞成分中，而在急性运动轴索性神经病中，神经轴突上的膜（轴膜）是免疫相关损伤的主要靶标。已经报道了 GBS 的暴发，最常见的与空肠弯曲菌感染有关，但其他因子，如寨卡病毒也与之密切相关。与感染相关的 GBS 患者常产生针对人周围神经神经节苷脂的抗体。相比之下，TM 是一种炎症性疾病，其特征为急性或亚急性运动、感觉和自主脊髓功能障碍。脊髓的横断面上存在上行和下行神经解剖通路的中断，类似于 GBS。它被认为是由感染因子和分子模拟触发的。在这篇综述中，我们将重点讨论感染因子作为 GBS 和 TM 触发因素的可能作用。
