Study of the pathogenic mechanisms of autoimmune myasthenia gravis - Case Study

Myasthenia gravis (MG) is an autoimmune disease caused by the presence of antibodies directed against components of the muscle membrane located at the neuromuscular junction. In the majority of cases, these are autoantibodies directed against the acetylcholine receptor (AChR). The origin of the autoimmune response is not known, but thymic abnormalities and defective regulation of the immune system certainly play a major role in patients with anti-AChR antibodies. It has thus been shown that environmental contaminants may be involved in the induction of myasthenia gravis via deregulation of pro-inflammatory Th17 lymphocytes via their AhR receptor. In the MG thymus, the balance of the couple composed of regulatory T lymphocytes (Treg) (anti-inflammatory) and Th17 lymphocytes plays an important role. Indeed, it has been suggested that the overexpression of cytokines IL-17 and IL-6 by Th17 could contribute to the maintenance of pathogenic inflammatory phenomena and to the production of autoantibodies.