Mechanism of action of voltage-gated K+ channel antibodies in acquired neuromyotonia.
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.
Tomimitsu
Hisanori
H
Third Department of Internal Medicine, Kagoshima University, Kagoshima, Japan.
Arimura
Kimiyoshi
K
Nagado
Tatsui
T
Watanabe
Osamu
O
Otsuka
Reika
R
Kurono
Asutsugu
A
Sonoda
Yoshito
Y
Osame
Mitsuhiro
M
Kameyama
Masaki
M
D000328:Adult; D001323:Autoantibodies / Q000494:pharmacology*; D045744:Cell Line, Tumor; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism / Q000494:pharmacology; D020386:Isaacs Syndrome / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D024642:Potassium Channels, Voltage-Gated / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism*; D018709:Statistics, Nonparametric
D001323:Autoantibodies; D007074:Immunoglobulin G; D024642:Potassium Channels, Voltage-Gated