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J Neuroimmunol. 2014 Nov 15;276(1-2):207-12. doi: 10.1016/j.jneuroim.2014.09.001. Epub 2014 Sep 16.

Autoantibodies to neurofascin-186 and gliomedin in multifocal motor neuropathy.

Author information

1
Department of Neuroscience and Imaging, University "G. d'Annunzio", Chieti-Pescara, Italy. Electronic address: francnotturno@yahoo.it.
2
Experimental Zooprophylactic Institute of Abruzzo and Molise "G. Caporale", Teramo, Italy.
3
Department of Medicine, National University of Singapore, Singapore; Department of Physiology, National University of Singapore, Singapore.
4
Institute for Research in Biomedicine, Bellinzona, Switzerland.
5
2nd Neurology, Department of Medical Biotechnology and Translational Medicine, IRCCS Humanitas Clinical Institute, Milan University, Rozzano, Milan, Italy.
6
Neurology Unit, Ospedale Treviglio, Bergamo, Italy.
7
Department of Respiratory Medicine, Catholic University, Rome, Italy.
8
Department of Neuroscience and Imaging, University "G. d'Annunzio", Chieti-Pescara, Italy.

Abstract

We tested autoantibodies to neurofascin-186 (NF186) and gliomedin in sera from patients with multifocal motor neuropathy (MMN, n=53) and chronic inflammatory demyelinating polyneuropathy (CIDP, n=95) by ELISA. IgG antibodies to NF186 or gliomedin were found in 62% of MMN and 1% of CIDP sera, and IgM antibodies to the same antigens in 12% of MMN and 1% of CIDP sera. These autoantibodies activated complement. Ten percent of the MMN sera without IgM anti-GM1 reactivity had anti-NF186 antibodies. Because NF186 and gliomedin play a crucial role for salutatory conduction, the autoantibodies may contribute to produce motor nerve conduction block and muscle weakness in MMN.

KEYWORDS:

Chronic inflammatory demyelinating neuropathy; Gliomedin; Multifocal motor neuropathy; Neurofascin

PMID:
25283719
DOI:
10.1016/j.jneuroim.2014.09.001
[Indexed for MEDLINE]

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