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

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

  • Notturno F Department of Neuroscience and Imaging, University "G. d'Annunzio", Chieti-Pescara, Italy. Electronic address: francnotturno@yahoo.it.
  • Di Febo T Experimental Zooprophylactic Institute of Abruzzo and Molise "G. Caporale", Teramo, Italy.
  • Yuki N Department of Medicine, National University of Singapore, Singapore; Department of Physiology, National University of Singapore, Singapore.
  • Fernandez Rodriguez BM Institute for Research in Biomedicine, Bellinzona, Switzerland.
  • Corti D Institute for Research in Biomedicine, Bellinzona, Switzerland.
  • Nobile-Orazio E 2nd Neurology, Department of Medical Biotechnology and Translational Medicine, IRCCS Humanitas Clinical Institute, Milan University, Rozzano, Milan, Italy.
  • Carpo M Neurology Unit, Ospedale Treviglio, Bergamo, Italy.
  • De Lauretis A Department of Respiratory Medicine, Catholic University, Rome, Italy.
  • Uncini A Department of Neuroscience and Imaging, University "G. d'Annunzio", Chieti-Pescara, Italy.
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  • 2014-10-07
Published in:
  • Journal of neuroimmunology. - 2014
Chronic inflammatory demyelinating neuropathy
Gliomedin
Multifocal motor neuropathy
Neurofascin
Animals
Autoantibodies
Cell Adhesion Molecules
Computational Biology
Enzyme-Linked Immunosorbent Assay
Female
G(M1) Ganglioside
Humans
Male
Membrane Proteins
Motor Neuron Disease
Nerve Growth Factors
Nerve Tissue Proteins
Polyneuropathies
Protein Isoforms
Rats
Transfection
English 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.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/210209
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