摘要
目的探究IL-2在调控巨噬细胞极化分型方面的作用及机制。方法重组小鼠白介素-2(IL-2)刺激处于M0期的小鼠单核巨噬细胞RAW 264.7,同时以IL-4作为对照。Real-time PCR和Western blot检测M1型和M2型标志分子的表达;流式细胞术检测M1型和M2型巨噬细胞的百分比;Western blot检测Jak3和Stat5活化水平。结果经IL-2刺激后,处于M0的RAW 264.7细胞显著上调表达M1型标记分子,如IL-1β、IL-12、TNF-α和i NOS等;IL-2使巨噬细胞中M1型的比例由3.2%上升到24.6%,同时Jak3和Stat5分子的磷酸化水平显著提高。结论 IL-2具有促进巨噬细胞由M0向M1极化的作用,且该作用可能是通过Jak3-Stat5通路实现。
Objective To explore the effects and related mechanisms of Interleukin-2 （IL-2） on macrophage polar- ization. Methods rmIL-2 was used to treat the mouse macrophage cells RAW 264.7. Then, the cell markers of M1 and M2 expression were detected by real-time PCR and Western blot. The percentage of M1 or M2 macrophages was analyzed by flow cytometry. Additionally, the activation of Jak3 and Star5 was also analyzed by Western blot. Results The expression of M1 maekers （IL-1β, IL-12, TNF-α and iNOS） was significantly up-regulated in RAW 264.7 cells after treatment with IL-2. IL-2 treatment increased the percentage of M1 macrophages from 3.2% to 24. 6%. IL-2 significantly enhanced the phosphorylation of Jak3 and StatS. Conclusions IL-2 promotes M1 polar- ization of macrophages, probably via the Jak3-Stat5 signaling pathway.
出处
《基础医学与临床》
CSCD
2015年第8期1055-1060,共6页
Basic and Clinical Medicine
基金
山东省科技发展计划(2012gsf11811)
