TWS119通过抑制STAT3磷酸化促进γδT细胞CCR5的表达  

TWS119 upregulates CCR5 expression of γδT cells by inhibiting STAT3 phosphorylation

作　　者：徐晶[1] 孙蕾清[1] 陈永强[1] 郑璐[1] 吕小婷[1] 陈复兴[1] 刘军权[1] 周忠海[1] 

机构地区：[1]解放军第97医院中心实验室,徐州221004

出　　处：《中国免疫学杂志》2016年第6期825-827,837,共4页Chinese Journal of Immunology

基　　金：南京军区医学科技创新研究基金(14MS032)资助

摘　　要：目的：研究糖原合酶激酶-3β抑制剂4,6-二取代吡咯并嘧啶（TWS119）促进γδT细胞趋化因子受体CCR5表达的分子机制。方法：用TWS119诱导从健康人外周血中分离培养获得γδT细胞48 h后,用流式细胞仪检测γδT细胞CCR5的表达;Western blot检测GAPDH和p-STAT3的表达。结果：培养10 d后的γδT细胞纯度达到85.79%±5.01%。TWS119浓度在0～8.0μmol/L范围内能显著促进趋化因子受体CCR5的表达,且剂量依赖性抑制STAT3的磷酸化。同时,用STAT3磷酸化抑制剂Stattic（0.5μmol/L）预处理γδT细胞也可以促进CCR5的表达,并能协同增强TWS119促进趋化因子受体CCR5的表达。结论：TWS119通过抑制STAT3磷酸化促进γδT细胞CCR5的表达。Objective：To investigate the mechanisms of TWS119 induced CCR5 expression in hunman γδT cells. Methods：After treatment with various concentrations of TWS119 for 48h, the expression of CCR5 in γδT cells were detected by flow cytometry. The p-STAT3 and GAPDH expression were examined by Western blot analysis. Results： TWS119 could upregulate the expression of CCR5 in dose dependent manner. Western blot analysis revealed that TWS119 inhibit phosphorylation of STAT3,but had no significant impact on GAPDH. In addition, pretreatment of γδT cells with 0. 5 μmol/L STAT3 specific phosphorylation inhibitor Stattic could upregulate the expression of CCR5 and enhance the TWS119 induced CCR5 expression. Conclusion： TWS119 could upregulate CCR5 expression of γδT cells by inhibiting STAT3 phosphorylation in vitro.

关 键 词：TWS119 CCR5 ΓΔT细胞 STAT3 

分 类 号：R392.12[医药卫生—免疫学] Q253[医药卫生—基础医学]