Shoenfeld Y, George J, Peter J B
Department of Medicine 'B', Sheba Medical Center, Tel Hashomer, Israel.
Int Arch Allergy Immunol. 1996 Apr;109(4):318-26. doi: 10.1159/000237258.
Guillain-Barré syndrome (GBS) entails a demyelinating process of the peripheral nervous system. The etiopathogenesis of the syndrome is still a matter of debate although considerable progress has been accomplished in the recent years. Abundant evidence has been put forward so as to support the role of the immune system in initiating and perpetuating the ongoing damage culminating in the emergence of the clinically overt syndrome. As such, data on the involvement of the humoral immune pathways add to the information already presented with regard to cell-mediated mechanisms participating in disruption of peripheral nerve. The following review will focus on the current knowledge of these complex mechanisms and the relative significance of each in the pathogenesis of GBS.
吉兰-巴雷综合征(GBS)涉及外周神经系统的脱髓鞘过程。尽管近年来已取得了相当大的进展,但该综合征的病因发病机制仍存在争议。已经提出了大量证据来支持免疫系统在启动和持续进行正在发生的损伤中所起的作用,这种损伤最终导致临床上明显综合征的出现。因此,关于体液免疫途径参与的相关数据补充了已有的关于参与外周神经破坏的细胞介导机制的信息。以下综述将聚焦于这些复杂机制的当前知识以及每种机制在GBS发病机制中的相对重要性。