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Treatment of Myasthenia Gravis by Preventing Acetylcholine Receptor Modulation
Author(s) -
Losen Mario,
MartínezMartínez Pilar,
Phernambucq Marko,
Schuurman Janine,
Parren Paul W.H.I.,
De Baets Marc H.
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1405.034
Subject(s) - myasthenia gravis , acetylcholine receptor , neuromuscular junction , autoantibody , antigen , receptor , acetylcholine , antibody , chemistry , postsynaptic potential , immunology , microbiology and biotechnology , endocrinology , medicine , neuroscience , biochemistry , biology
Myasthenia gravis (MG) is an autoimmune disease caused by antibodies mainly directed to the acetylcholine receptor (AChR) of the neuromuscular junction. Induction of antigenic modulation and complement activation by such autoantibodies leads to ultrastructural damage of the postsynaptic membrane and loss of AChR and associated proteins. Reduction of antigenic modulation by increasing the expression of the receptor‐associated anchor protein, rapsyn, or by functionally monovalent competing IgG4 anti‐AChR antibodies was shown to prevent MG disease activity. We propose that preventing antigenic modulation can be used as a treatment strategy for MG.