{"title":"[AChR 抗体阳性肌萎缩症]。","authors":"Hiroyuki Murai","doi":"10.11477/mf.1416202651","DOIUrl":null,"url":null,"abstract":"<p><p>Herein, we describe the mechanisms, diagnostic procedures, and treatment options for acetylcholine receptor (AChR) antibody-positive myasthenia gravis (MG). The upstream pathomechanism of this condition involves AChR-sensitized T cell-dependent B cell proliferation and the subsequent production of pathogenic autoantibodies. Downstream molecules include AChR antibodies that activate complement pathways, resulting in the destruction of motor endplates. We further introduce newly-developed molecular targeted drugs for the treatment of MG that aims to secure patients' health-related quality of life.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":"76 5","pages":"613-620"},"PeriodicalIF":0.0000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[AChR Antibody-Positive Myasthenia Gravis].\",\"authors\":\"Hiroyuki Murai\",\"doi\":\"10.11477/mf.1416202651\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Herein, we describe the mechanisms, diagnostic procedures, and treatment options for acetylcholine receptor (AChR) antibody-positive myasthenia gravis (MG). The upstream pathomechanism of this condition involves AChR-sensitized T cell-dependent B cell proliferation and the subsequent production of pathogenic autoantibodies. Downstream molecules include AChR antibodies that activate complement pathways, resulting in the destruction of motor endplates. We further introduce newly-developed molecular targeted drugs for the treatment of MG that aims to secure patients' health-related quality of life.</p>\",\"PeriodicalId\":52507,\"journal\":{\"name\":\"Brain and Nerve\",\"volume\":\"76 5\",\"pages\":\"613-620\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brain and Nerve\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.11477/mf.1416202651\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain and Nerve","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11477/mf.1416202651","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
摘要
在此,我们将介绍乙酰胆碱受体(AChR)抗体阳性重症肌无力(MG)的发病机制、诊断程序和治疗方案。这种疾病的上游病理机制包括乙酰胆碱受体敏感的 T 细胞依赖性 B 细胞增殖以及随后产生的致病性自身抗体。下游分子包括激活补体途径的 AChR 抗体,从而导致运动终板的破坏。我们进一步介绍了新开发的治疗 MG 的分子靶向药物,旨在确保患者与健康相关的生活质量。
Herein, we describe the mechanisms, diagnostic procedures, and treatment options for acetylcholine receptor (AChR) antibody-positive myasthenia gravis (MG). The upstream pathomechanism of this condition involves AChR-sensitized T cell-dependent B cell proliferation and the subsequent production of pathogenic autoantibodies. Downstream molecules include AChR antibodies that activate complement pathways, resulting in the destruction of motor endplates. We further introduce newly-developed molecular targeted drugs for the treatment of MG that aims to secure patients' health-related quality of life.