Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy

PLoS One. 2015 Jul 28;10(7):e0134274. doi: 10.1371/journal.pone.0134274. eCollection 2015.

Abstract

Multifocal motor neuropathy is an immune mediated disease presenting with multifocal muscle weakness and conduction block. IgM auto-antibodies against the ganglioside GM1 are detectable in about 50% of the patients. Auto-antibodies against the paranodal proteins contactin-1 and neurofascin-155 and the nodal protein neurofascin-186 have been detected in subgroups of patients with chronic inflammatory demyelinating polyneuropathy. Recently, auto-antibodies against neurofascin-186 and gliomedin were described in more than 60% of patients with multifocal motor neuropathy. In the current study, we aimed to validate this finding, using a combination of different assays for auto-antibody detection. In addition we intended to detect further auto-antibodies against paranodal proteins, specifically contactin-1 and neurofascin-155 in multifocal motor neuropathy patients' sera. We analyzed sera of 33 patients with well-characterized multifocal motor neuropathy for IgM or IgG anti-contactin-1, anti-neurofascin-155 or -186 antibodies using enzyme-linked immunosorbent assay, binding assays with transfected human embryonic kidney 293 cells and murine teased fibers. We did not detect any IgM or IgG auto-antibodies against contactin-1, neurofascin-155 or -186 in any of our multifocal motor neuropathy patients. We conclude that auto-antibodies against contactin-1, neurofascin-155 and -186 do not play a relevant role in the pathogenesis in this cohort with multifocal motor neuropathy.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Animals
  • Autoantibodies / blood*
  • Autoantibodies / immunology
  • Case-Control Studies
  • Cell Adhesion Molecules / immunology*
  • Contactin 1 / immunology*
  • Female
  • HEK293 Cells
  • Humans
  • Male
  • Mice, Inbred C57BL
  • Middle Aged
  • Muscle Fibers, Skeletal / metabolism
  • Nerve Growth Factors / immunology*
  • Polyneuropathies / blood*
  • Polyneuropathies / immunology
  • Polyneuropathies / pathology
  • Prospective Studies
  • Protein Isoforms

Substances

  • Autoantibodies
  • CNTN1 protein, human
  • Cell Adhesion Molecules
  • Contactin 1
  • NFASC protein, human
  • Nerve Growth Factors
  • Protein Isoforms

Grant support

The study was supported by research funds of the University of Würzburg. LA is supported by a grant of the Graduate School of Life Sciences of the University of Würzburg. Work in the laboratory of SDH and SGW was supported in part by grants from the Rehabilitation Research Service and Medical Research Service, Department of Veterans Affairs, United States of America.