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目的探讨高迁移率蛋白B1(HMGB1)促进白细胞介素(IL)-2转录表达免疫效应的分子机制。方法构建HMGB1和活化T细胞核因子2(NFAT2)的真核表达质粒,分别单独转染以及共同转染人胚胎肾细胞系293T、人子宫颈癌细胞系Hela,同时转染IL-2报告基因,检测IL-2报告基因的表达活性。观察当HMGB1与NFAT2质粒共同转染细胞时,是否能协同促进IL-2报告基因的活性。结果在293T细胞中,HMGB1或NFAT2单独转染可提高活性倍数相加为6.8倍,而二者共转时报告基因活性与未刺激对照组相比提高了18.4倍。在Hela细胞中,二者单独转染可提高活性倍数相加为49.9倍,而二者共转时报告基因活性与未刺激对照组相比提高了117.7倍。结论HMGB1可与NFAT2可协同促进IL-2报告基因转录表达。
Objective To investigate the molecular mechanism of high mobility protein B1 (HMGB1) on the immune effect of interleukin (IL) -2 transcription. Methods Eukaryotic expression plasmids of HMGB1 and NFAT2 were constructed and transfected into human embryonic kidney cell line 293T and human cervical cancer cell line Hela respectively and transfected with IL-2 reporter gene. The expression activity of the IL-2 reporter gene was detected. To investigate whether HMGB1 and NFAT2 co-transfected cells could synergistically promote IL-2 reporter gene activity. Results In 293T cells, the single transfection with HMGB1 or NFAT2 increased the activity multiples by 6.8 times, and the reporter gene co-transfection increased the reporter gene activity by 18.4 folds compared with the untreated control. In Hela cells, the two transfection alone increased the activity fold to 49.9 fold, while the two transfection time reporter gene activity compared with unstimulated control group increased by 117.7 times. Conclusion HMGB1 can cooperate with NFAT2 to promote the transcription of IL-2 reporter gene.