儿童过敏性紫癜发病中NF-κB对树突状细胞的调控与T辅助细胞分化失衡的关系

陶红; 李秋; 王莉佳; 张高福; 王莉; 李翠萃; 阳海平

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儿童过敏性紫癜发病中NF-κB对树突状细胞的调控与T辅助细胞分化失衡的关系

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- 儿童过敏性紫癜发病中NF-κB对树突状细胞的调控与T辅助细胞分化失衡的关系
- Correlation between regulation of dendritic cells by nuclear transcription factor-κB and imbalance of T helper cell differentiation in pathogenesis of henoch-schonlein purpura during childhood
- 陆军军医大学学报 2010年32卷第23期页码：2519-2523
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  中图分类号： R554.602;R392.11;R392.3
- 纸质出版：2010
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陶红,李秋,王莉佳,张高福,王莉,李翠萃,阳海平.儿童过敏性紫癜发病中NF-κB对树突状细胞的调控与T辅助细胞分化失衡的关系[J].陆军军医大学学报(原第三军医大学学报),2010,32(23):2519-2523.

　Tao Hong,Li Qiu,Wang Lijia,Zhang Gaofu,Wang Li,Li Cuicui,Yang Haiping.Correlation between regulation of dendritic cells by nuclear transcription factor-κB and imbalance of T helper cell differentiation in pathogenesis of henoch-schonlein purpura during childhood[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(23):2519-2523.
陶红,李秋,王莉佳,张高福,王莉,李翠萃,阳海平.儿童过敏性紫癜发病中NF-κB对树突状细胞的调控与T辅助细胞分化失衡的关系[J].陆军军医大学学报(原第三军医大学学报),2010,32(23):2519-2523. DOI：

　Tao Hong,Li Qiu,Wang Lijia,Zhang Gaofu,Wang Li,Li Cuicui,Yang Haiping.Correlation between regulation of dendritic cells by nuclear transcription factor-κB and imbalance of T helper cell differentiation in pathogenesis of henoch-schonlein purpura during childhood[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(23):2519-2523. DOI：

摘要

目的了解儿童过敏性紫癜发病中NF-κB对树突状细胞的调控与T辅助细胞分化失衡的关系。方法收集我院2008年6月至2009年3月肾脏免疫科收治的过敏性紫癜(henochschonlein purpura，HSP)患儿36例和过敏性紫癜肾炎（henochschonlein purpura nephritis，HSPN)患儿32例，以及门诊体检的健康儿童27例，抽取外周血

诱导培养树突状细胞（dendritic cells

DC），于第5天分别抽取7例以上3组外周血诱导培养的DC加入NF-κB抑制剂5 μg，分别采用ELISA、流式细胞技术、RT-PCR和细胞免疫化学方法，检测患儿血浆IL-4、INF-γ和DC培养上清IL-12、IL-10水平；DC表面CD

、CD

、CD-209的表达；DC内NF-κB亚型p50、p65 mRNA表达量和NF-κB活化情况。结果与对照组比较，HSP组和HSPN组血浆中Th2类细胞因子IL-4升高（P0.05），Th1类细胞因子INF-γ降低（P0.05）；DC培养上清中IL-10升高（P0.05），IL-12降低（P0.05）；CD

、CD

升高（P0.05），CD

降低（P0.05）；细胞内NF-κB p50、p65 mRNA 表达量也升高（P0.05）；NF-κB活化表达数量增多。但HSP组与HSPN组以上检测指标2组比较差异无统计学意义（P0.05）。加入NF-κB抑制剂后以上各项异常指标可逆转，且逆转后与对照组比较差异无统计学意义（P0.05）。结论 HSP发病与DC异常调控Th1/Th2细胞失衡密切相关，NF-κB是DC免疫功能的关键性调控基因，抑制NF-κB的活化是阻断DC功能和依赖于T细胞免疫反应的一个有效靶点。

Abstract

Objective To study the correlation between regulation of dendritic cells（DC）by nuclear transcription factor-κB and imbalance

of T helper cell differentiation in pathogenesis of henoch-schonlein purpura (HSP) during childhood. Methods Thirty-six children with HSP and 32 children with henoch-schonlein purpura nephritis (HSPN) admitted to our hospital in June 2008 to March 2009 and 27 healthy children enrolled in this study

served as HSP group

HSPN group and control group

respectively. Peripheral blood was drawn from 7 children in each group on day 5 to culture DC

into which 5 μg of NF-κB inhibitors was added. The levels of IL-4

INF-γ in plasma and IL-12

IL-10 in supernatant of cultured DC were measured by ELISA

flow cytometry

RT-PCR and cellular immunochemistry

respectively. Expressions of CD

，CD

，CD-209

NF-κB isoforms p50 and p65 mRNA as well as activation of NF-κB in DC were also detected by ELISA

flow cytometry

RT-PCR and cellular immunochemistry

respectively. Results The IL-4 level was higher and the INF-γ level was lower in HSP and HSPN groups than in control group (P0.05). The IL-10 level in supernatant of cultured DC and the IL-4 level in plasma were significantly higher in HSP and HSPN groups than in control group(P0.05). The expression level of CD

and CD

was significantly higher while that of CD

was significantly lower in HSP and HSPN groups than in control group(P0.05). The expression level of NF-κB p50 and p65 mRNA was also higher in HSP and HSPN groups than in control group (P0.05). No significant difference was observed in activation of NF-κB between HSP and HSPN groups. The above abnormal parameters could return to normal when NF-κB inhibitors were added into the cultured DC

with no difference among the three groups. Conclusion The pathogenesis of HSP is closely related with the abnormal regulation of DC and imbalance of Th1/ Th2 cells. NF-κB is a key regulatory gene of DC immune function

thus inhibiting the activation of NF-κB is a valid target to block DC function depending on T-cell immune response.

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