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J Neuroimmunol. 2014 Dec 15;277(1-2):13-7. doi: 10.1016/j.jneuroim.2014.09.012. Epub 2014 Sep 18.

Antibodies to neurofascin exacerbate adoptive transfer experimental autoimmune neuritis.

Author information

1
Neuroinflammation Group, Brain & Mind Research Institute, University of Sydney, Sydney, Australia.
2
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.
3
Department of Neurology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
4
Neuroinflammation Group, Brain & Mind Research Institute, University of Sydney, Sydney, Australia. Electronic address: emily.mathey@sydney.edu.au.

Abstract

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.

KEYWORDS:

Autoantibody; Chronic inflammatory demyelinating polyneuropathy; Guillain–Barré syndrome; Neurofascin; Nodes of Ranvier

PMID:
25262157
DOI:
10.1016/j.jneuroim.2014.09.012
[Indexed for MEDLINE]

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