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机构地区:[1]南方医科大学南方医院皮肤科,广东广州510515
出 处:《南方医科大学学报》2009年第10期2138-2139,共2页Journal of Southern Medical University
基 金:中华医学会皮肤病学分会科研基金课题
摘 要:目的探讨转录因子T-bet和GATA-3在系统性红斑狼疮(SLE)发病中的作用。方法采用逆转录多聚酶链反应(RT-PCR)测定60例SLE患者及20例正常对照组外周血单一核细胞(PBMC)T-bet和GATA-3mRNA表达状况。结果SLE患者组、活动期SLE患者组及非活动期SLE患者组T-betmRNA相对表达水平均明显低于正常对照组,相反GATA-3mRNA相对表达水平则明显高于正常对照组。结论GATA-3高表达促使初始T细胞向Th2细胞分化,诱导分泌Th2型细胞IL-6、IL-10等,同时抑制T-bet,导致Th1的低表达,从而促使B细胞处于高活化状态产生大量自身抗体,导致多种组织器官的损伤,寻找有效方法调控SLE患者体内GATA-3的表达,将为治疗SLE开辟一条新途径。Objectives To investigate the role of transcription factors T-bet and GATA-3 in the pathogenesis of systemic lupus erythematosus (SLE). Methods The expression of T-bet and GATA-3 mRNA in the peripheral blood mononuclear cells (PBMCs) of 60 patients with SLE and 20 normal control subjects were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results Compared with the normal controls, T-bet mRNA expression decreased whereas GATA-3 mRNA expression increased significantly in patients with SLE, active SLE and inactive SLE. Conclusions The high expression of GATA-3 promotes the immature T cells to differentiate into Th2 cells, induces Th2 cells to secrete the cytokines IL-6 and IL-10, which, along with the low expression of Thl as a result ofT-bet expression inhibition, causes B cell activation to produce a large quantity of autoantibodies, leading finally to multiple organ injuries. Effective regulation of GATA-3 expression may provide a new clue for the treatment of SLE.
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