CD4^+CD25^+调节性T细胞及其转录因子FoxP3在儿童过敏性紫癜发病机制中的作用  

The role of transcription factors FoxP3 and CD^4+CD25^+ regulatory T cells in pathogenesis of childhood Hench-Schonlein purpura

作　　者：王强[1] 任淑红[2] 董巍[3] 房俊[3] 

机构地区：[1]四川省人民医院儿科,成都610072 [2]郑州市第一人民医院儿科,450004 [3]四川省人民医院临床医学中心实验室,成都610072

出　　处：《中国小儿血液与肿瘤杂志》2012年第1期17-19,共3页Journal of China Pediatric Blood and Cancer

基　　金：四川省卫生厅科研课题提供资助(编号303005002209044)

摘　　要：目的探讨CD4+CD25+调节性T细胞(Treg)及其转录因子FoxP3在儿童过敏性紫癜(HSP)发病机制中的作用。方法研究对象为我院儿科2009年2月-2010年2月收治的急性期HSP患儿46例(HSP组)以及健康对照儿童30例(对照组)。采用SYBR GreenⅠ实时荧光定量PCR方法检测外周血单个核细胞FoxP3 mRNA的表达。运用流式细胞术检测外周血中CD4+CD25+Treg的表达。结果 HSP组患儿外周血单个核细胞FoxP3 mRNA相对表达水平(32.17±23.04)低于对照组(147.91±99.15)(P<0.01)。CD4+CD25+Treg占淋巴细胞比例HSP组[(5.34±2.51)%]低于对照组[(7.85±1.97)%],两组比较差异有显著性(P﹤0.01)。CD4+CD25+Treg与FoxP3 mRNA的表达呈正相关(r=0.502,P=0.01)。结论 HSP患儿急性期存在CD4+CD25+Treg的表达降低,其特异性的转录因子FoxP3 mRNA表达下调。Treg的减少以及由此引发的免疫抑制效应不足,可能是HSP急性期免疫失衡的重要原因之一。Objective To investigate the role of transcription factors FoxP3 and CD4^＋CD25^＋ regulatory T cells in the pathogenesis of childhood Hench-Schonlein purpura.Methods Real-time PCR was used to measure the mRNA levels of FoxP3 in 46 HSP patients（HSP group） and 30 healthy children（control group）.Besides,flow cytometry was used to detect the expression of CD4^＋CD25^＋ in peripheral blood mononuclear cells in HSP and control groups.Results The relative mRNA levels of FoxP3 in HSP group（32.17±23.04） were lower than those in control group（147.91±99.15）（P0.01）.The expression levels of CD4^＋CD25^＋ in HSP group（5.34±2.51）% were higher than those in control group（7.85±1.97）%（P〈0.01）.Conclusions The expression of CD4^＋CD25^＋ regulatory T cells and FoxP3 decreased in acute phase of childhood HSP,which indicated that the insufficiency of immunosuppressive effects caused by the regulatory T cells reduction might be an important reason of immunity imbalance in HSP acute phase.This study provides some experimental evidence in the pathogenesis of childhood Hench-Schonlein purpura.

关 键 词：FOXP3 CD4+CD25+调节性T细胞 过敏性紫癜 儿童 

分 类 号：R725.5[医药卫生—儿科]