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The Cur­rent View of Im­munopathogenesis of Myasthenia Gravis


Authors: M. Jakubíková 1;  J. Piťha 1,2
Authors‘ workplace: Neurologická klinika a Centrum klinických neurověd, 1. LF UK a VFN v Praze 1;  MS Centrum Teplice, Neurologické oddělení, Krajská zdravotní, a. s. – Nemocnice Teplice o. z. 2
Published in: Cesk Slov Neurol N 2015; 78/111(6): 649-654
Category: Review Article

Overview

Myasthenia gravis (MG) is an autoimmune disease that results in failure of neuromuscular transmission. Earlier theories of the dominant role of pathologic autoantibodies against target antigens (nicotinic acetylcholine receptor, muscle-specific tyrosine kinase and low-density lipoprotein receptor) were corrected following discovery of immune dysregulation at the level of T cells – between Th1 and Th2 and/or between T regulatory cells and Th17 cells, proliferation of CD8+ lymphocytes, chemokines, cytokines and other molecules. The immune system dysfunction can occur at different levels of the immune response: helper CD4+ T cells, cytotoxic CD8+ T cells, regulatory CD4+CD25+ T lymphocytes, Th17 lymphocytes, B lymphocytes and plasma cells. Thymus plays a dominant immunopathogenetic role in younger patients with MG, while extrathymic mechanisms are applied in older patients. Different immunologic mechanisms play a role in MG associated with a thymoma.

Key words:
myasthenia gravis – thymus – autoantibodies – T lymphocytes – B lymphocytes – cytokines

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.


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