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Myasthenia gravis: recognition of a human autoantigen at the molecular level
Institution:1. School of Metallurgy and Environment, Central South University, Changsha 410083, China;2. Key laboratory of Hunan Province for Metallurgy and Material Processing of Rare Metals, Changsha 410083, China;1. ATVS - Biometric Recognition Group, EPS, Universidad Autonoma de Madrid, Spain;2. da/sec - Biometrics and Internet Security Research Group, Hochschule Darmstadt, Germany;3. Inst. for the Protection and Security of the Citizen, European Commission - JRC, Italy;4. NISlab, Norwegian University of Science and Technology, NTNU, Gjøvik, Norway;1. School of Economics and Management, University of Science and Technology Beijing, Beijing, China;2. School of Accounting, Southwestern University of Finance and Economics, Chengdu, China;3. School of Economics and Management, Beijing Institute of Petrochemical Technology, Beijing, China;4. Chinese Academy of Social Sciences, Institute of Finance, Beijing, China
Abstract:The symptoms of myasthenia gravis are primarily or exclusively due to an autoimmune response against the muscle nicotinic acetylcholine receptor (AChR) and this has been the object of intensive investigations for almost 20 years. A detailed picture at the molecular level of the interaction of this autoantigen with the key elements involved in the autoimmune response, such as anti-AChR antibodies, the T-cell receptor and restricting major histocompatibility complex molecules, is now emerging for both human myasthenia gravis and its experimental model, experimental autoimmune myasthenia gravis. Here, Maria Pia Protti and colleagues focus on the molecular interactions occurring in human myasthenia gravis and summarize recent information on pathogenic mechanisms of the autoimmune response, and the structure of epitopes recognized by B cells and CD4+T cells of myasthenic patients on the AChR molecule.
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