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作 者:李山山 王皓[1] 周海舟[1] LI Shanshan;WANG Hao;ZHOU Haizhou(Department of Clinical Laboratory,the First Affiliated Hospital of Harbin Medical University,Harbin 150001,China)
机构地区:[1]哈尔滨医科大学第一附属医院检验科,哈尔滨150001
出 处:《国际免疫学杂志》2024年第1期94-98,共5页International Journal of Immunology
摘 要:类风湿性关节炎(rheumatoid arthritis,RA)是一种伴有多个关节肿、痛、畸形的免疫性疾病,严重情况下会引起关节功能的严重障碍,现已证实成纤维样滑膜细胞(fibroblast-like synoviocytes,FLS)与RA有极强的关联性,RA-FLS在RA发病机制中起关键作用。RA-FLS可自行产生多种炎性细胞因子,也可被某些细胞因子或物质刺激而产生多种炎性细胞因子,这些炎性细胞因子可增加RA-FLS的侵袭性和增殖能力,并减少RA-FLS的凋亡,从而进一步加重关节炎。文章重点探讨了几种可对RA-FLS产生影响的细胞因子,以期为治疗RA提供新的思路。Rheumatoid arthritis(RA)is an immune disease with multiple joint swelling,pain and deformity,which can cause severe impairment of joint function in severe cases.Fibroblast-like synoviocytes(FLS)have been shown to have a strong association with RA,and plays a key role in the pathogenesis of RA.RA-FLS can produce a variety of inflammatory cytokines on its own,and also can be stimulated by certain cytokines or substances to produce a variety of inflammatory cytokines.These inflammatory cytokines can increase the aggressiveness and proliferative ability of RA-FLS and reduce the apoptosis of RA-FLS,thereby further aggravating arthritis.This review focuses on several cytokines that can have an impact on RA-FLS,in order to provide new ideas for the treatment of RA.
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