Yan Weixing, Nguyen Toan, Yuki Nobuhiro, Ji Qiuhong, Yiannikas Con, Pollard John D, Mathey Emily K
Neuroinflammation Group, Brain & Mind Research Institute, University of Sydney, Sydney, Australia.
Departments of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
J Neuroimmunol. 2014 Dec 15;277(1-2):13-7. doi: 10.1016/j.jneuroim.2014.09.012. Epub 2014 Sep 18.
Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy are autoimmune disorders of the peripheral nervous system in which autoantibodies are implicated in the disease pathogenesis. Recent work has focused on the nodal regions of the myelinated axon as potential autoantibody targets. Here we screened patient sera for autoantibodies to neurofascin and assessed the pathophysiological relevance of anti-neurofascin antibodies in vivo. Levels of anti-neurofascin antibodies were higher in sera from patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy when compared with those of controls. Anti-neurofascin antibodies exacerbated and prolonged adoptive transfer experimental autoimmune neuritis and caused conduction defects when injected intraneurally.
格林-巴利综合征和慢性炎症性脱髓鞘性多发性神经病是外周神经系统的自身免疫性疾病，其中自身抗体与疾病发病机制有关。最近的研究工作聚焦于有髓轴突的节点区域作为潜在的自身抗体靶点。在此，我们筛查了患者血清中针对神经束蛋白的自身抗体，并评估了抗神经束蛋白抗体在体内的病理生理相关性。与对照组相比，格林-巴利综合征和慢性炎症性脱髓鞘性多发性神经病患者血清中的抗神经束蛋白抗体水平更高。抗神经束蛋白抗体加剧并延长了过继转移实验性自身免疫性神经炎，并且当经神经内注射时会导致传导缺陷。
