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From the Department of Neurology, Baylor College of Medicine, and the Veterans Administration Medical Center, Houston, TX.
We used cultured myotubes to demonstrate complement-dependent lysis of muscle membranes by serum from patients with myasthenia gravis. Lysis was monitored by light microscopy and release of incorporated [86Rb]. In the presence of guinea pig complement (GPC), 18 of 37 heat-inactivated myasthenic sera (49%), but none of 16 controls, caused morphologically detectable myotube lysis. Ten of 19 myasthenic sera (53%) increased [86Rb]-release compared with 10 controls. Immunoglobulin fractions retained the complement-dependent lytic activity. Inactivation of GPC prevented the lysis. [86Rb]-release appeared to correlate with clinical severity. The complement-dependent lysis resulted in a decrease in the number of acetylcholine receptors (AChRs) in myotubes, and AChR-immunoglobulin complexes were found in the medium of lysed cultures. The data suggest that cultured myotubes can be used to document complement-dependent antibody reactions in the pathogenesis of myasthenia.
Address correspondence and reprint requests to Dr. Ashizawa, Department of Neurology, Baylor College of Medicine, 6501 Fannin, Houston, TX 77030.
Supported by grants from the Veterans Administration; the Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation; and the John A. Hartford Foundation.
Presented in part at the thirty-sixth annual meeting of the American Academy of Neurology, Boston, MA, April 1984.
Accepted for publication April 1, 1985.
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