2008/06/01 by Mario Losen, Pilar Martínez‐Martínez, Marko Phernambucq +3 · 1 citation
Medicine · #Myasthenia Gravis and Thymoma #Peripheral Neuropathies and Disorders #Antifungal resistance and susceptibility
paper · doi:10.1196/annals.1405.034
openalex publication_date 2008/06/01 · openalex created_date 2016/06/24 · openalex updated_date 2026/07/03
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.