国家自然科学基金资助项目(30471538)和浙江省医药卫生科学研究基金 (2005-B472).
This work was supported by a grant from The National Natural Science Foundation of China (30471538) and Medical Health of Zhejiang (2005-B472).
树突状细胞表面特异的胞间黏附分子3捕获非整合素(DC-specific intercellular adhesion molecule-3-grabbing nonintegrin,DC-SIGN) 是树突状细胞表面特异的蛋白,在抗原呈递过程中起关键作用.这种特异性的表达和DC-SIGN的调节机制有关.到目前为止, DC-SIGN 表达调控的机制还不是很清楚.IL-4是诱导DC-SIGN表达的最重要的细胞因子之一,而NF-κB是调控细胞信号转导的一个重要调控因子,两者都和DC-SIGN的表达调节相关.研究了IL-4和NF-κB对DC-SIGN启动子活性、对DC-SIGN表达的影响以及IL-4和NF-κB之间相互作用的关系.发现:DC-SIGN启动子中NF-κB位点缺失可以使DC-SIGN启动子活性下降大约50%, NF-κBp50可以促进DC-SIGN在THP-1细胞的表达,IL-在THP-1细胞诱导DC-SIGN表达的同时,也促进了NF-κBp50的表达.这些结果显示,在THP-1细胞中NF-κBp50参与IL-4诱导的DC-SIGN表达.
DC-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) is specific receptor on Dendritic cells, and plays a pivotal role on antigens presentation. Uptodate, the clear regulation mechanisms for DC-SIGN expression are not available. IL-4 is one of the most important cytokines inducing DC-SIGN production, while, NF-κB is an important transcription factor controlling signaling transduction. Both IL-4 and NF-κB are closely related to DC-SIGN regulation. NF-κB and IL-4 actions on DC-SIGN promoter activity, DC-SIGN expression as well as interactions between IL-4 and NF-κB were investigated in THP-1 cell. It was found that the mutation of NF-κB binding site in DC-SIGN promoter results in DC-SIGN promoter activity decrease about 50%. NF-κBp50 stimulates DC-SIGN expression in THP-1 cells. IL-4 upregulates DC-SIGN expression on THP-1 cells as well as NF-κB production. These data reveal that NF-κB is associated with IL-4 induced DC-SIGN expression.
许利军,常秀春,姚航平,吴南屏. NF-κBp50参与IL-4在THP-1细胞中诱导DC-SIGN的表达[J].生物化学与生物物理进展,2008,35(1):50-55
复制生物化学与生物物理进展 ® 2024 版权所有 ICP:京ICP备05023138号-1 京公网安备 11010502031771号