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In the first part of the present study we compared the antigenicity of affinity-purified acetylcholine receptors from the cell line TE671 and from human skeletal muscle. The reactivities of the two acetylcholine receptor preparations showed a strong correlation (r = 0.96) in a radioimmunoassay using sera from myasthenia gravis patients. In additional functional studies, carbamylcholine stimulated cAMP production in TE671 cells to 130%. This increase was even more pronounced when TE671 cells were grown in the presence of dexamethasone. alpha-Bungarotoxin completely blocked this carbamylcholine-induced cAMP increase. Using the Ca2+ indicator, indo-1, it was shown that intracellular Ca2+ concentrations ([Ca2+]i) were elevated in TE671 cells after stimulation with carbamylcholine. This effect was also completely blocked by alpha-bungarotoxin. To test the functional activity of autoantibodies against the acetylcholine receptor, TE671 cells were preincubated with sera from myasthenia gravis patients. In one third of sera a significant inhibition of the agonist-stimulated [Ca2+]i increase was detected, possibly caused by antibodies directed to functionally important areas of the acetylcholine receptor. There was no correlation between the inhibition rate of [Ca2+]i and anti-acetylcholine receptor antibody titres in these patient sera.

Immunological and Functional Properties of the Acetylcholine Receptor Expressed on the Human Cell Line TE671