Anti-CD20 monoclonal antibodies in multiple sclerosis

被引:40
|
作者
Moreno Torres, Irene [1 ]
Garcia-Merino, Antonio [1 ]
机构
[1] Puerta de Hierro Majadahonda Univ Hosp, Dept Neurol, Neuroimmunol Unit, Madrid, Spain
关键词
Multiple sclerosis; B lymphocytes; B cells; monoclonal antibodies; anti-CD20; neuroimmunology; meningeal inflammation; B-CELL DEPLETION; SYSTEMIC-LUPUS-ERYTHEMATOSUS; PATIENTS RECEIVING RITUXIMAB; ANTIVIRAL IMMUNE-RESPONSE; EPSTEIN-BARR-VIRUS; CEREBROSPINAL-FLUID; T-CELLS; MENINGEAL INFLAMMATION; INTRATHECAL RITUXIMAB; RHEUMATOID-ARTHRITIS;
D O I
10.1080/14737175.2017.1245616
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction: The therapeutic utility of the anti-CD20 monoclonal antibodies (mAbs) is currently being evaluated in multiple sclerosis (MS) in line with the better understanding of the role of B lymphocytes in MS pathogenesis. Area covered: We conducted a literature search using Medline/Pub Med database of basic research and available controlled trials about anti-CD20 mAbs in MS. Additionally, ongoing studies were identified in the ClinicalTrials.gov database. B cells exert multiple inflammatory and regulatory functions playing an important role in MS pathogenesis as is demonstrated by the production of autoantibodies, infiltration of B cells in MS lesions and the formation of ectopic B cell follicle-like structures in meninges, among others. B-cell depletion by anti-CD20 mAbs has been shown to have an impact on these pathogenic mechanisms. The efficacy of three of them, rituximab, ocrelizumab and ofatumumab in MS has been confirmed by placebo-controlled clinical trials demonstrating a significant reduction of the annualized relapsing rate (ARR), new gadolinium-enhancing (GdE) and T2 lesions. There have been no significant safety problems so far but the overall benefit to risk profile is still to be determined. Expert commentary: After recent good results of these agents in MS therapy, questions related to maintenance therapy, markers of response and control of B cells values remain unanswered.
引用
收藏
页码:359 / 371
页数:13
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