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T-Cell Derived Mechanisms in the Pathogenesis of Myasthenia Gravis

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Epithelial Tumors of the Thymus
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Abstract

Myasthenia gravis (MG) is often described as the prototype of an auto antibody-mediated autoimmune disease. The autoantibodies are directed against the nicotinic acetylcholine receptor on the skeletal muscle endplate, the disease is transmitted from mother to child and from humans to animals, and immunisation with acetylcholine receptor induces experimental myasthenia gravis in animals.1 The disease-specific autoantibodies are, however, found in conditions not accompanied by neuromuscular symptoms, as in healthy first-degree relatives to patients, in monoclonal gammopathies, in primary biliary cirrhosis and in thymomas. Despite extensive efforts to try to distinguish the disease-causing antibodies found in myasthenia with those found in other conditions, no clear difference between these antibodies has been found. These observations together with the rather bad correlation between the concentration of autoantibodies in serum and the clinical symptoms suggest that mechanisms other than these antibodies may contribute by modulating the effects of autoantibodies on the neuromuscular junction.

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Lefvert, A.K. (1997). T-Cell Derived Mechanisms in the Pathogenesis of Myasthenia Gravis. In: Marx, A., Müller-Hermelink, H.K. (eds) Epithelial Tumors of the Thymus. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0033-3_27

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  • DOI: https://doi.org/10.1007/978-1-4899-0033-3_27

  • Publisher Name: Springer, Boston, MA

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