• Medientyp: E-Artikel
  • Titel: Mechanism of action of voltage‐gated K+ channel antibodies in acquired neuromyotonia
  • Beteiligte: Tomimitsu, Hisanori; Arimura, Kimiyoshi; Nagado, Tatsui; Watanabe, Osamu; Otsuka, Reika; Kurono, Asutsugu; Sonoda, Yoshito; Osame, Mitsuhiro; Kameyama, Masaki
  • Erschienen: Wiley, 2004
  • Erschienen in: Annals of Neurology
  • Sprache: Englisch
  • DOI: 10.1002/ana.20221
  • ISSN: 0364-5134; 1531-8249
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  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>Acquired neuromyotonia (ANM) is associated with antibodies to voltage‐gated K<jats:sup>+</jats:sup> channels (VGKCs). ANM sera reduce the number of K<jats:sup>+</jats:sup> currents in neuronal cell lines, but it is not clear how the antibodies act. Here, we show by using the NB‐1 cell line that the reduction in K<jats:sup>+</jats:sup> currents by IgG is independent of added complement. IgG Fc and Fab fragments from ANM sera had no effect, but three of four ANM F(ab′)<jats:sub>2</jats:sub> fragments significantly reduced K<jats:sup>+</jats:sup> currents. Thus, cross‐linking of the channels by divalent antibodies is likely to be an important mechanism in reducing K<jats:sup>+</jats:sup> currents. Ann Neurol 2004;56:440–444</jats:p>