过敏性紫癜患儿外周血单核细胞TLR2表达及其与Th1和Th2型免疫应答相关性研究

发布时间：2018-03-18 18:28

本文选题：过敏性紫癜　切入点：紫癜性肾炎　出处：《青岛大学》2013年硕士论文　论文类型：学位论文

【摘要】：目的探讨TLR2在过敏性紫癜患儿外周血单核细胞的表达及其与Thl和Th2型免疫应答的相关性,探讨TLR2在HSP发病机制的作用。方法选取2011年10月-2012年11月于我院收治的过敏性紫癜患儿64例为研究对象,分为HSP无肾损害组(NHSPN,36例)及HSP有肾损害组(HSPN,28例),另选取我院儿保科健康查体儿童30例作为正常对照组。采用流式细胞术检测外周血单核细胞TLR2蛋白表达阳性率,实时荧光定量PCR技术检测外周血单核细胞TLR2-mRNA的基因相对表达量,ELISA法检测血浆IFN-γ、IL-4水平。两组间比较采用t检验,多组间比较采用单因素方差分析和LSD-t检验,相关分析采用Pearson相关检验进行统计学处理。结果1.HSP患儿外周血单核细胞(peripheral blood mononuclear cells, PBMC) TLR2mRNA相对表达量及TLR2蛋白表达率均显著高于正常对照组(t’=4.283,P0.01；t’=5.487,P0.01),HSPN组外周血单核细胞TLR2mRNA相对表达量及TLR2蛋白表达率均明显高于NHSPN组(F=9.32,P0.05；F=21.522,P0.01)；2.HSP组血浆IL-4水平显著高于对照组((t'=13.446,P0.01),IFN-γ水平显著低于对照组(t'=14.364,P0.01),IFN-γ/IL-4比值显著低于对照组(t=7.410,P0.01)。3.HSP组CD4+T细胞TLR2蛋白表达率TLR2mRNA呈正相关；与血浆IL-4水平呈显著正相关；与IFN-γ/IL-4比值呈显著负相关；与血浆IFN-y水平不存在相关性。结论1.HSP患儿外周血单核细胞TLR2mRNA及蛋白表达均明显增高；HSP有肾损害组患儿外周血单核细胞TLR2mRNA及蛋白表达皆显著高于HSP无肾损害组。2. HSP病儿存在Th1/Th2失衡,Th2优势活化与TLR2蛋白表达升高呈显著相关。3.TLR2活化可能参与了HSP的免疫发病机制,TLR2的过度活化可能与HSP的肾损伤有关。。
[Abstract]:Objective to investigate the expression of TLR2 in peripheral blood monocytes of children with Henoch-Schonlein purpura and its correlation with Thl and Th2 type immune response, and to explore the role of TLR2 in the pathogenesis of HSP. Methods Sixty-four children with Henoch-Schonlein purpura from October 2011 to November 2012 were selected as subjects. The positive rate of TLR2 protein expression in peripheral blood monocytes was detected by flow cytometry (FCM) in 30 healthy children in our hospital and 30 healthy children in our hospital as the control group. The positive rate of TLR2 protein expression in peripheral blood mononuclear cells was detected by flow cytometry, and the positive rate of TLR2 protein expression in peripheral blood monocytes was detected by flow cytometry, and the positive rate of TLR2 protein expression in peripheral blood monocytes was detected by flow cytometry. The relative expression of TLR2-mRNA gene in peripheral blood monocytes was detected by real-time fluorescence quantitative PCR and the plasma level of IFN- 纬 -IL-4 was detected by Elisa. T test was used for the comparison between the two groups, and univariate ANOVA and LSD-t test were used for the comparison between the two groups. Correlation analysis was performed by Pearson correlation test. Results 1. The relative expression of TLR2mRNA and the expression rate of TLR2 protein in peripheral blood monocyte blood mononuclear cells of children with HSPN were significantly higher than those in the normal control group (4.283) P0.01P0.01P0.01HSPN and the expression rate of TLR2mRNA and TLR2 protein in peripheral blood monocytes of HSPN group were significantly higher than that of NHSPN group. 2. The relative expression of TLR2mRNA and the expression rate of TLR2 protein in peripheral blood monocytes of HSPN group were significantly higher than those of NHSPN group. 2. The level of plasma IL-4 in the control group was significantly higher than that in the control group (P < 0.01). The level of IFN- 纬 was significantly lower than that of the control group (P < 0.01). The ratio of IFN- 纬 / IL-4 in the control group was significantly lower than that in the control group. The expression rate of TLR2 protein on CD4 T cells in the control group was significantly lower than that in the control group. There was significant positive correlation with plasma IL-4 level, negative correlation with IFN- 纬 / IL-4 ratio, and no correlation with plasma IFN-y level. Conclusion 1. The expression of TLR2mRNA and protein in peripheral blood monocytes in children with HSP2 was significantly higher than that in children with renal damage caused by HSP2. The expression of TLR2mRNA and protein in peripheral blood monocytes of children with HSP2 was significantly higher than that in patients with HSP without renal damage. 2. There was Th1/Th2 imbalance and Th2 dominant activation in children with HSP. The activation of TLR2 may be involved in the immune pathogenesis of HSP. The overexpression of TLR2 may be related to the renal injury of HSP.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R725.5

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