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作 者:耿旭强 吴歆[1] 徐沪济[1] GENG Xu-qiang;WU Xin;XU Hu-ji(Department of Rheumatology and Immunology,Changzheng Hospital,Naval Medical University(Second Military Medical University),Shanghai 200003,China)
机构地区:[1]海军军医大学(第二军医大学)长征医院风湿免疫科,上海200003
出 处:《第二军医大学学报》2021年第3期308-313,共6页Academic Journal of Second Military Medical University
基 金:国家自然科学基金(31770988)。
摘 要:类风湿关节炎(RA)是一种常见的慢性自身免疫性疾病,其发病机制尚未完全阐明。研究发现,B细胞数量和功能异常在RA发生、发展中发挥着重要作用。B细胞通过抗体依赖和非抗体依赖等多种途径参与RA的发生和发展,阐明这些途径的分子机制将为RA治疗药物的开发提供新的靶点。本文主要综述了B细胞功能紊乱与RA发病的关系,为全面理解RA发病机制、寻找新的治疗靶点提供思路。Rheumatoid arthritis(RA)is a common chronic autoimmune disease,and its pathogenesis remains to be fully elucidated.Recent evidences suggested that the abnormal count and the dysfunction of B cells played important roles in the development and progression of RA.B cells participate in the development and progression of RA through antibody dependent and independent pathways,and elucidating the specific molecular mechanisms of these pathways will provide new targets for the development of RA therapeutic drugs.This paper reviews the relationship between the B-cell dysfunction and the pathogenesis of RA,providing references for a comprehensive understanding of the pathogenesis of RA and exploring new therapeutic targets.
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