机构地区:[1]青岛大学医学院附属医院心肾免疫儿科,266003 [2]青岛市市立医院儿内科
出 处:《中华实用儿科临床杂志》2014年第21期1648-1651,共4页Chinese Journal of Applied Clinical Pediatrics
基 金:山东省优秀中青年科学家科研奖励基金(BS2011SW006);山东省医药卫生科技发展计划项目(2011HW029)
摘 要:目的观察过敏性紫癜(HSP)患儿外周血树突状细胞(DC)表面Toll样受体(TLR)2、TLR3、TLR4表达状况,探讨TLR表达异常在HSP免疫发病机制中的作用。方法选择2011年12月至2012年7月在青岛大学医学院附属医院住院治疗的HSP患儿20例为HSP组,20例健康体检儿童为健康对照组。无菌条件下采集外周静脉抗凝血,密度梯度离心法分离获得外周血单个核细胞(PBMC),体外经细胞因子重组人粒细胞.巨噬细胞集落刺激因子(rhGM-CSF)、重组人白细胞介素4(rhlL-4)和重组人肿瘤坏死因子-α(rhTNF-α)诱导培养获得DC,采用流式细胞仪检测DC表面TLR2、TLR3、TLR4、CD83、CD86的表达。结果1.HSP组DC表面CD83表达率与健康对照组比较差异无统计学意义(t=0.80,P〉0.05)。2.HSP组DC表面CD86表达率显著高于健康对照组(t=9.56,P〈0.01)。HSP组DC表面TLR2、TLR3、TLR4表达率均明显高于健康对照组(t=11.79、13.29、9.45,P均〈0.01)。3.HSP组DC表面TLR2、TLR3、TLR4表达率与CD86表达率皆呈正相关(r=0.84,P〈0.01;r=0.53,P〈0.05;r=0.66,P〈0.05)。结论HSP患儿DC表面TLR2、TLR3、TLR4和共刺激分子CD86表达增强且呈正相关,提示TLR和共刺激分子表达异常在HSP发病机制中起重要作用,可能通过启动以Th2为优势的异常免疫应答参与HSP的发病。Objective To observe the expression of Toll-like receptor(TLR) on peripheral blood dendritic cells(DC) in children with Henoch-Schonlein purpura(HSP),and to investigate the pathogenesis of the abnormal expression of TLR in children with HSP. Methods Twenty hospitalized children with HSP in the Affiliated Hospital of Qingdao University Medical College from Dec. 2011 to Jul. 2012 were enrolled in the study( HSP group). Twenty agemetched healthy children were selected as a healthy control group. Peripheral venous blood was sampled under aseptic condition,peripheral blood mononnclear cells (PBMC) were isolated from density gradient centrifugation,and DC were generated by recombinat human granulocyte-macrophage colony-stimulating factor(GM-CSF) , interleukin-4( IL-4 ) and tumor necrosis factor-α(TNF-α) in vitro. Expressions of CDs3, CD86 and TLR2, TLR3, TLR4 in peripheral blood DC were examined by fluorescent activated cell sorter (FACS). Results 1. No significant distinction was found in the expression of the CD83 on peripheral blood DC between HSP group and healthy control group ( t = 0.80, P 〉 0.05 ) ;in HSP group had remarkably increased expression of the CD86 on peripheral blood DC than that of the healthy control group (t = 9.56 ,P 〈 0.01 ). 2. Expression rates of TLR2 ,TLR3 ,TLR4 on peripheral blood DC in the HSP group were higher than those in the healthy control group ( t = 11.79,13.29,9.45, all P 〈 0.01 ). 3. Expression rates of TLR2, TLR3 and TLR4 in HSP group had positive correlation with expression rates of CD86 ( r = 0.84, P 〈 0.01 ; r = 0.53, P 〈 0.05 ; r = 0.66,P 〈 0.05 ). Conclusions Expressions of TLR2, TLR3 and TLR4 on peripheral blood DC significantly increased and were positively correlated with expression of CDa6. This implies that TLR and co-stimulatory molecules might participate in the pathogenesis of HSP by mediating signal transduction, leading to abuormity of cytokines, then inducing Th1/Th2 immune imbalance by showing the ad
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