Abstract
High-affinity IgG autoantibodies to muscle nicotinic acetylcholine receptors (AChRs) were discovered to cause myasthenia gravis (MG) and its animal model more than 30 years ago (Patrick and Lindstrom, 1973; Lindstrom et al ., 1976 a , b ; Vincent et al ., 2006), and the antigenic structure of muscle AChRs is still being actively investigated (Kalamida et al ., 2007; Lindstrom et al ., 2008). Immune precipitation of AChRs tagged in their acetylcholine-binding sites with 125I-labelled α−bungarotoxin provided a sensitive immunodiagnostic assay for MG (Lindstrom et al ., 1976 b ). However, up to 20% of those who appeared to have autoimmune MG, because they benefited from plasmapheresis or exhibited antibodies bound to their neuromuscular junctions, did not have autoantibodies detectable by the conventional assay (Vincent et al ., 2006). Angela Vincent and her co-workers discovered that about half of the putative seronegative MG patients actually had autoantibodies to muscle-specific …
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