摘要
目的探讨树突状细胞(dendritic cell,DC)在小儿过敏性紫癜(Henoch-Schnlein purpura,HSP)发病中的可能作用及机制。方法采集33例过敏性紫癜患儿和20例正常对照组儿童的外周血,以Thomas法,采用粒-巨噬细胞集落刺激因子、白介素4(IL-4)和肿瘤坏死因子-α(TNF-α)联合培养诱导DC细胞,检测DC协同刺激分子B7-1(CD80)、B7-2(CD86)的表达,及其分泌的IL-6、IL-12水平的变化。结果过敏性紫癜患儿外周血DC分泌IL-6水平[(274.4±51.2)ng/L]明显高于对照组[(154.3±46.4)ng/L],差异有高度统计学意义(t=8.05,P<0.01);外周血DC分泌IL-12水平[(89.6±17.7)ng/L]明显低于对照组[(129.4±18.2)ng/L],差异有高度统计学意义(t=6.03,P<0.01);同时过敏性紫癜患儿外周血协同刺激分子B7-2(CD86)的表达水平(51.2±7.4)明显高于对照组(37.3±6.5),差异有高度统计学意义(t=7.92,P<0.01)。结论DC可能通过诱导Th1/Th2细胞分化在小儿过敏性紫癜发病中起重要作用,其可能的机制系通过DC细胞分泌的细胞因子而起作用。
Objectives To investigate the pathogenesis of dendritic cell （DC） in children with Henoch-Schnlein purpura （HSP）. Methods The method adopted by Thomas was modified. The adherent precursors of DC were isolated from peripheral blood in children with HSP and healthy children. The adherent cells were induced and DC were generated by granulocyte-macrophage colony-stimulating factor （GM-CSF）, interleukin-4 （IL-4） and tumor necrosis factor-α （TNF- α） in vitro. The expression of CD80, CD86 on the DC was examined by fluorescent activated cells sorter （FACS）, and the secretion of IL-6, IL-12 was significantly detected. Results Compared with healthy children, the secretion of IL-6 was significantly increased （P 〈 0.01）, the secretion of IL-12 was significantly decreased （P 〈 0.01）, and the co-stimulating factor CD86 （B7-2） expressed by DC was remarkably increased （P 〈 0.01） in children with HSP. Conclusions DC may play a vital role in the immunological mechanism of HSP by means of inducing the imbalance of Th1 / Th2, the possible mechanism may involve the interleukins （especially IL-6 and IL-12, etc.） secreted by DC.
出处
《临床儿科杂志》
CAS
CSCD
北大核心
2009年第1期58-60,共3页
Journal of Clinical Pediatrics
基金
兰州大学医学科研基金资助项目(No.LZUYX200662)
