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NEUROLOGY 1989;39:1057
© 1989 American Academy of Neurology

Anti-acetylcholine receptor antibodies block bungarotoxin binding to native human acetylcholine receptor on the surface of TE671 cells

Andrew R. Pachner, MD

Department of Neurology, Georgetown University School of Medicine, Washington, DC.

We assayed sera from 20 myasthenics of various clinical stages and anti-acetylcholine receptor (AChR) antibody levels for their ability to affect bungarotoxin (BGT) binding to native human AChR on the surface of TE671 cells. Thirty-five percent of sera blocked BGT binding to the AChR, some at a dilution of up to 1:1000. The 7 patients whose sera blocked toxin binding were all generalized myasthenics with particularly severe disease, 6 of whom had had myasthenic crisis at some point in their course. No ocular myasthenics had blocking antibody. Blockade of toxin binding by myasthenic antibody to TE671 cells resembled blockade produced by unlabeled toxin in being irreversible with washing. There was little correlation between ability to block toxin binding and amplitude of the AChR binding antibody. These data are consistent with the hypothesis that patients with more aggressive generalized myasthenia preferentially have anti-AChR antibody that blocks toxin binding.

Address correspondence and reprint requests to Dr. Pachner, Georgetown University School of Medicine, Department of Neurology, 3800 Reservoir Road, Washington, DC 20007.

Supported by a grant from the National Institute of Neurological and Communicative Disorders and Stroke (NS 23538).

Received November 16, 1988. Accepted for publication in final form February 16, 1989.






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