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作 者:刘慧敏[1] 马军格[1] 张西克[1] 范凌云[1] 耿静[1] 张美莲[1]
机构地区:[1]河北工程大学附属医院皮肤科,河北石家庄056000
出 处:《皮肤病与性病》2010年第4期2-3,共2页Dermatology and Venereology
摘 要:目的探讨Toll样受体-9(Toll like receptor-9,TLR9)介导系统性红斑狼疮(systemic lupus erythematosus,SLE)患者产生抗dsDNA抗体的分子机制,以寻找治疗SLE的新的药物作用靶位。方法实验分为三组,即实验组:以SLE患者的外周血单一核细胞(Peripheral blood mononuclear cell,PBMC)为靶细胞,用MyD88依赖的MyD88/IRAKs/TRAF6/NIK/NF-κB经典路径的拮抗剂R-848阻断该路径,再用天然的小牛胸腺DNA作为免疫原刺激PBMC,用ELISA法检测细胞培养上清液中的抗dsD-NA抗体;未干预组:以SLE患者的外周血单一核细胞(Peripheral blood mononuclear cell,PBMC)为靶细胞,用天然的小牛胸腺DNA作为免疫原刺激PBMC,用ELISA法检测细胞培养上清液中的抗dsDNA抗体;对照组:以SLE患者的外周血PBMC为靶细胞,加入等量的生理盐水至上述培养基中,用ELISA法检测细胞培养上清液中的抗dsDNA抗体。结果加R-848组产生抗dsDNA抗体水平明显低于未加R-848组,两组间比较有显著性差异(P<0.05)。结论 TLR9介导的抗dsDNA抗体产生是经由MyD88依赖的MyD88/IRAKs/TRAF6/NIK/NF-κB经典路径发生的。Objective To investigate the molecular mechanism of anti-dsDNA antibody production in patients with systemic lupus erythematosus for looking for the new target site in SLE treatment.Methods In experimental group,peripheral blood mononuclear cell(PBMC) from patients with SLE was blocked by R-848,then stimulated by nCTDNA;in intervention group,PBMC was only stimulated by nCTDNA;in control group,PBMC was cultured with normalsaline,the level of anti-dsDNA antibody in supernatant of all groups was measured by ELISA.Results Compared with intervention group,the level of anti-dsDNA antibody in R-848 treated group was significantly lower(P0.05).Conclusions Production of TLR9-induced anti-dsDNA antibody was dependent on MyD88/IRAKs/TRAF6/NIK/NF-κB signaling pathway.
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