Schröder A, Ellrichmann G, Chehab G, Schneider M, Linker R A, Gold R
Neurologische Klinik, St. Josef Hospital, Ruhr-Universität Bochum, 44791, Bochum, Deutschland.
Nervenarzt. 2009 Feb;80(2):155-6, 158-60, 162-5. doi: 10.1007/s00115-008-2663-3.
Rituximab, a human-mouse chimeric CD20 monoclonal antibody that depletes CD20-positive B cells, has already demonstrated efficacy in hematologic and rheumatologic diseases. Treatment with rituximab results in depletion of CD20-positive cells via multiple mechanisms, including complement-mediated or antibody-dependent cytotoxicity and apoptosis. Recent histopathologic and immunologic studies reveal an influence of B cells on the development and perpetuation of many chronic inflammatory diseases of the nervous system. Promising results with rituximab were already reported in the therapy of myasthenia gravis, immunoneuropathies, neuromyelitis optica, and multiple sclerosis, in which first controlled studies have been recently published. In this review we summarize available data from these reports and also discuss possible underlying molecular mechanisms.
利妥昔单抗是一种人鼠嵌合型CD20单克隆抗体,可清除CD20阳性B细胞,已在血液学和风湿病疾病中显示出疗效。利妥昔单抗治疗可通过多种机制导致CD20阳性细胞的清除,包括补体介导的或抗体依赖性细胞毒性以及细胞凋亡。最近的组织病理学和免疫学研究揭示了B细胞对许多神经系统慢性炎症性疾病的发生和持续存在的影响。利妥昔单抗在重症肌无力、免疫性神经病、视神经脊髓炎和多发性硬化症的治疗中已报告有令人鼓舞的结果,最近已发表了首批对照研究。在本综述中,我们总结了这些报告中的现有数据,并讨论了可能的潜在分子机制。