Thymus Myasthenia gravis

Balandina A, Lecart S, Dartevelle P, Saoudi A, Berrih-Aknin S Functional defect of regulatory CD4+CD25+T cells in the thymus of patients with autoimmune myasthenia gravis. Blood 2005 105 735-741. 

More than 90% of patients with myasthenia gravis have circulating antibodies directed against a subunit of the acetylcholine receptor/ Immunosuppressive drugs and steroids help to cut down on these autoantibodies, and many patients are benefit-ted by removal of the thymus. Newer approaches involve specific immunotherapy aimed at increasing tolerance to either T cells or to B cells.C/d For example, oral ingestion of purified acetylcholine receptors to desensitize the body s response or inhibition of production of 11-2. 

Pathogenesis. The clinical features of myasthenia gravis are caused by specific autoantibodies to the nicotinic acetylcholine receptor. These antibodies accelerate receptor turnover shortening their typical lifetime in the skeletal muscle membrane from aroimd 7 days to 1 day in a myasthenic. This process results in marked depletion of receptors from myasthenic skeletal muscle (about 90%) explaining its fatigability. The frequent finding of a specific haplotype (Al-B8-Dw3 HLA) in myasthenics and concurrent hyperplasia or tumours of the thymus support the autoimmune basis for the disease. 

Nagane Y, Utsugisawa Obara D, Tohgo H (2001) NKT-associated markers and perforin in hyperplastic thymuses from patients with Myasthenia gravis. Muscle Nerve 24 1359-1364. 

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