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Myasthenia Gravis Conference: A Summation

An international conference devoted to myasthenia gravis research is held by the Academy every five years. The 50 platform presentations and better than 100 poster presentations given at this meeting attest to the intensity of the ongoing effort. Each participant comes away from a meeting such as this with certain general perceptions of what has been accomplished over the past five years and, it is hoped, some unique ones that will guide his or her future efforts. I believe I speak for all in remarking that it is gratifying to note how far our understandings of myasthenia gravis, of allied disorders, and of the structure and function of the acetylcholine receptor have advanced over the past five years. In this brief postlude I can mention only a few of the highlights of this meeting as I see them. Without question the progress made in studying the structure and function of the acetylcholine receptor represents a signal accomplishment. The recently developed, powerful methods of molecular biology have made this possible. The entire sequence of all four chains of the receptor has been deduced, and this has led to testable hypotheses as to the mechanisms involved in ion-channel opening and closing. With the sequence known, it has been possible to synthesize peptides spanning areas of particular interest, and these have already proved useful in determining the sites of alpha-bungarotoxin binding and the locations of epitopes that activate B cells and T cells (which epitopes appear to differ from one another); in delineating hitherto dimly perceived distinctions between junctional and extrajunctional receptors; and in clarifying the changes that occur with denervation. It is well to point out that, while receptor sequences have been deduced for several species, including man, the provocative suggestion was advanced at this congress that subtle differences in receptor structure may exist between strains of experimental animals of the same species, and perhaps between one person and another as well. Such differences, if they exist, could bear on the safety factor, which could conceivably, for this reason alone, vary between individuals. These differences could also bear on the poor correlation observed between measured antibody titer and severity of disease in myasthenia gravis, inasmuch as an antibody directed against an epitope unique to an individual might not be detected by routine assays for antibody to the acetylcholine receptor. An understanding of the basis for the Lambed-Eaton syndrome has emerged over the past few years and was extensively documented at this meeting. The disease is almost surely antibody mediated, as attested to by successful adoptive transfer of the disease to experimental animals by administered immunoglobulin from Lambert-Eaton-syndrome patients. The antibody in question has been shown to cross-link structures of the terminal axon and to disrupt calcium influx, which in turn impedes release