| 书目名称 | Myasthenia Gravis | | 副标题 | Disease Mechanism an | | 编辑 | Premkumar Christadoss (Professor) | | 视频video | | | 图书封面 |  | | 描述 | Autoimmune myasthenia gravis (MG) is a classical autoimmunedisease, for which the target antigen, nicotinic acetylcholinereceptor, has been cloned, sequenced and biochemically characterized.Antibodies to acetylcholine receptors destroy acetylcholine receptorat the neuromuscular junction, thus leading to defective neuromusculartransmission, muscle fatigue, and weakness. .In the last few years, rapid advances have been made in unraveling thecellular and molecular mechanisms involved in the pathogenesis of MG,both in the animal model, experimental autoimmune MG (EAMG), and inhuman MG. Significant advances are being made in characterizing thecells and molecules involved in the autoimmune response to theacetylcholine receptor (AChR). These advances are leading to thedevelopment of specific methods of immunointervention in EAMG. Furtherunderstanding of the intricate involvement of the majorhistocompatibility complex (MHC) and non-MHC genes, T cell receptors(TCR), costimulator molecules, and specific cytokines in the afferentand efferent autoimmune response of AChR should pave the way to futureantigen/clone-specific therapy of MG. .This book is the outcome of the MG workshop proceedings i | | 出版日期 | Book 2000 | | 关键词 | Antigen; T cell; Thymus; autoimmune disease; blood; cell; clinical trial; cytokine; histocompatibility; muscl | | 版次 | 1 | | doi | https://doi.org/10.1007/978-94-011-4060-7 | | isbn_softcover | 978-94-010-5787-5 | | isbn_ebook | 978-94-011-4060-7 | | copyright | Springer Science+Business Media Dordrecht 2000 |
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发表于 2025-3-21 18:46:42
