Lu sur : https://www.ncbi.nlm.nih.gov/pubmed/31269763
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Cells. 2019 Jul 2;8(7). pii: E671. doi: 10.3390/cells8070671.
Myasthenia Gravis: Pathogenic Effects of Autoantibodies on Neuromuscular Architecture.
Koneczny I1, Herbst R2.
Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction (NMJ). A
utoantibodies target key molecules at the NMJ, such as the nicotinic acetylcholine receptor (AChR), muscle-specific kinase (MuSK), and low-density lipoprotein receptor-related protein 4 (Lrp4), that lead by a range of different pathogenic mechanisms to altered tissue architecture and reduced densities or functionality of AChRs, reduced neuromuscular transmission, and therefore a severe fatigable skeletal muscle weakness.
In this review, we give an overview of the history and clinical aspects of MG, with a focus on the structure and function of myasthenic autoantigens at the NMJ and how they are affected by the autoantibodies' pathogenic mechanisms.
Furthermore, we give a short overview of the cells that are implicated in the production of the autoantibodies and briefly discuss diagnostic challenges and treatment strategies.
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