Acetylcholine Receptors and Myasthenia Gravis

Abstract

Conclusions

This review has dealt with recent advances in the understanding of myasthenia gravis. The fundamental abnormality affecting the neuromuscular junctions of myasthenic patients is a reduction of ACh receptors, due to an autoimmune attack directed against the receptors. Antibodies to ACh receptors are present in most patients, and there is evidence that they have a path-ogenetic role in the disease. The mechanism of antibody action involves acceleration of the rate of degradation of ACh receptors, attributable to crosslinking of the receptors by the antibody. In addition, antibodies produce blocking of the ACh receptors. The possibility that cell-mediated mechanisms may participate in the immune responses in some myasthenic patients remains to be explored. Perhaps the most important gap in the present understanding of myasthenia gravis concerns the origin of the autoimmune process, although there is in direct evidence that the thymus gland may be involved. Future research will be directed toward developing therapeutic methods to deal with the specific immunological abnormalities of individual myasthenic patients.

The original work carried out in the author's laboratory was supported by Grants 5 PO1 NS10920 and 5 RO1 HD04817 from the National Institutes of Health and by grants from the Muscular Dystrophy Association, Inc., and the Myasthenia Gravis Foundation.