Abstract
Two important observations in 1973 resulted in a breakthrough in Myasthenia Gravis (MG) research. The first by Fambrough et al [1] showed reduced levels of acetylcholine receptor (AChR) at the neuromuscular junction of patients with MG and the second, by Patrick and Lindstrom [2], demonstrated that rabbits immunized with AChR develop an autoimmune response to AChR, resulting in muscle weakness, and a decrementai electromyogram response to repeated nerve stimulation, which are characteristic to MG. These two pivotal observations were seminal for elucidating and understanding the autoimmune nature of MG, and prompted a vast amount of research into both MG and its experimental animal model, experimental autoimmune myasthenia gravis (EAMG).
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Fuchs, S., Im, SH., Barchan, D., Souroujon, M.C. (2000). Antigen-Specific Therapy of Experimental Autoimmune Myasthenia Gravis: Mucosal tolerance with recombinant fragments of the human acetylcholine receptor. In: Christadoss, P. (eds) Myasthenia Gravis. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4060-7_16
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DOI: https://doi.org/10.1007/978-94-011-4060-7_16
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