Plasma from myasthenia gravis patients reduces acetylcholine receptor agonist-induced Na+ flux into TE671 cell line.
Plasma from myasthenia gravis patients was tested for its ability to inhibit agonist-induced 22Na+ influx into the TE671 cell line that expresses human acetylcholine receptors. Reduced 22Na+ influx correlated weakly with the total anti-acetylcholine receptor antibody level in the plasma, and was also related to the presence of antibody directed against the agonist binding site, as detected by inhibition of 125I-alpha-bungarotoxin binding. However, in some cases there was inhibition of 22Na+ flux without evident anti-alpha-bungarotoxin binding site antibody. We conclude that in most patients antibodies that interfere with 22Na+ influx do so by blocking the agonist binding site. However, in some cases antibodies may be directed at the Na+ ion channel or some important functional determinant.
Lang
B
B
Department of Neurological Science, Royal Free Hospital, London, U.K.
Richardson
G
G
Rees
J
J
Vincent
A
A
Newsom-Davis
J
J
D000328:Adult; D001323:Autoantibodies / Q000276:immunology; D001692:Biological Transport; D002038:Bungarotoxins / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D005260:Female; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D008297:Male; D009157:Myasthenia Gravis / Q000276:immunology*; D011978:Receptors, Nicotinic / Q000276:immunology* / Q000502:physiology; D012964:Sodium / Q000502:physiology; D014407:Tumor Cells, Cultured
D001323:Autoantibodies; D002038:Bungarotoxins; D007473:Ion Channels; D011978:Receptors, Nicotinic; D002217:Carbachol; D012964:Sodium