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目的初步探讨PKCθ在结核杆菌抗原(MtbAg)刺激γδT细胞转录因子NFκB活化中的作用。方法 MtbAg刺激健康人外周血单个核细胞(PBMC),获得γδT细胞优势扩增细胞群。PKCθ选择性阻断剂rottlerin(粗糠柴毒素)预处理,MtbAg刺激γδT细胞,通过凝胶电泳迁移率变动分析(EMSA)检测γδT细胞NFκB活性,流式细胞术(FCM)检测γδT细胞活化分子CD69的表达。结果 MtbAg刺激30min,γδT细胞NFκB活性逐渐增加,刺激60min时NFκB活性显著增强;rottlerin使Mt-bAg激发的γδT细胞NFκB活性明显减弱。Rottlerin可显著抑制MtbAg诱导的γδT细胞活化分子CD69的表达(P<0.01)。结论 PKCθ参与MtbAg诱导的γδT细胞转录因子NFκB活化。
Objective To investigate the role of PKCθ in the activation of γδ T cell transcription factor NFκB stimulated by Mycobacterium tuberculosis antigen (MtbAg). Methods MtbAg was used to stimulate peripheral blood mononuclear cells (PBMCs) of healthy people to obtain the dominant population of expanded γδT cells. ΓδT cells were stimulated by MtbAg, EMSA was used to detect the NFκB activity in γδT cells, and flow cytometry (FCM) was used to detect the activation of γδT cells CD69 expression. Results MtbAg stimulation 30min, γδT cells NFκB activity gradually increased, stimulated NFκB activity significantly increased 60min; rottlerin Mt-bAg-induced γδT cells NFκB activity was significantly weakened. Rottlerin significantly inhibited MtbAg-induced CD69 expression of γδT cells (P <0.01). Conclusion PKCθ is involved in MtbAg-induced NF-κB activation in γδT cells.