{"title":"单克隆抗体治疗视神经脊髓炎","authors":"Woojun Kim","doi":"10.59578/jmsni.2023.14.1.15","DOIUrl":null,"url":null,"abstract":"Neuromyelitis optica spectrum disorder (NMOSD) is caused by antibodies that target the aquaporin-4 (AQP4) water channel expressed on astrocytes. Specific antibody binding to AQP4 produces complement-dependent cytotoxicity, resulting in inflammation and demyelination. New biologic treatments demonstrate high efficacy and good safety for patients with AQP4-immunoglobulin G-positive NMOSD. They were eculizumab, an anti-complement C5 antibody, satralizumab, an anti-interleukin-6 receptor antibody, and inebilizumab and rituximab, which targets CD19 and CD20, respectively, causing depletion of B-cells. In this review, the pathophysiology of NMOSD, the methodology and results of the recent studies examining monoclonal antibody therapies, and the optimal therapeutic strategy for NMOSD were covered.","PeriodicalId":324885,"journal":{"name":"Journal of Multiple Sclerosis and Neuroimmunology","volume":"88 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Monoclonal Antibody Therapies for Neuromyelitis Optica Spectrum Disorder\",\"authors\":\"Woojun Kim\",\"doi\":\"10.59578/jmsni.2023.14.1.15\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Neuromyelitis optica spectrum disorder (NMOSD) is caused by antibodies that target the aquaporin-4 (AQP4) water channel expressed on astrocytes. Specific antibody binding to AQP4 produces complement-dependent cytotoxicity, resulting in inflammation and demyelination. New biologic treatments demonstrate high efficacy and good safety for patients with AQP4-immunoglobulin G-positive NMOSD. They were eculizumab, an anti-complement C5 antibody, satralizumab, an anti-interleukin-6 receptor antibody, and inebilizumab and rituximab, which targets CD19 and CD20, respectively, causing depletion of B-cells. In this review, the pathophysiology of NMOSD, the methodology and results of the recent studies examining monoclonal antibody therapies, and the optimal therapeutic strategy for NMOSD were covered.\",\"PeriodicalId\":324885,\"journal\":{\"name\":\"Journal of Multiple Sclerosis and Neuroimmunology\",\"volume\":\"88 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-06-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Multiple Sclerosis and Neuroimmunology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.59578/jmsni.2023.14.1.15\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Multiple Sclerosis and Neuroimmunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.59578/jmsni.2023.14.1.15","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Monoclonal Antibody Therapies for Neuromyelitis Optica Spectrum Disorder
Neuromyelitis optica spectrum disorder (NMOSD) is caused by antibodies that target the aquaporin-4 (AQP4) water channel expressed on astrocytes. Specific antibody binding to AQP4 produces complement-dependent cytotoxicity, resulting in inflammation and demyelination. New biologic treatments demonstrate high efficacy and good safety for patients with AQP4-immunoglobulin G-positive NMOSD. They were eculizumab, an anti-complement C5 antibody, satralizumab, an anti-interleukin-6 receptor antibody, and inebilizumab and rituximab, which targets CD19 and CD20, respectively, causing depletion of B-cells. In this review, the pathophysiology of NMOSD, the methodology and results of the recent studies examining monoclonal antibody therapies, and the optimal therapeutic strategy for NMOSD were covered.