Mechanism of action of voltage-gated K+ channel antibodies in acquired neuromyotonia.

Abstract

Acquired neuromyotonia (ANM) is associated with antibodies to voltage-gated K+ channels (VGKCs). ANM sera reduce the number of K+ 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+ 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')2 fragments significantly reduced K+ currents. Thus, cross-linking of the channels by divalent antibodies is likely to be an important mechanism in reducing K+ currents.

• Authors: Hisanori Tomimitsu, Kimiyoshi Arimura, Tatsui Nagado, Osamu Watanabe, Reika Otsuka, Asutsugu Kurono, Yoshito Sonoda, Mitsuhiro Osame, Masaki Kameyama
• Journal: Annals of neurology (Ann Neurol) Vol. 56 Issue 3 Pg. 440-4 (Sep 2004) ISSN: 0364-5134 [Print] United States
• PMID: 15349875 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Autoantibodies
• Immunoglobulin G
• Potassium Channels, Voltage-Gated

Topics

• Adult
• Autoantibodies (pharmacology)
• Cell Line, Tumor
• Female
• Humans
• Immunoglobulin G (metabolism, pharmacology)
• Isaacs Syndrome (immunology, metabolism)
• Male
• Middle Aged
• Potassium Channels, Voltage-Gated (antagonists & inhibitors, immunology, metabolism)
• Statistics, Nonparametric