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目的研究IFN-α对CD56+NK细胞的细胞因子分泌、杀伤功能和细胞内信号传导的作用。方法分离健康人PBMC分别与培养液、IFN-α和IL-12培养,利用酶联免疫吸附法(ELISA)检测培养上清中IFN-γ的水平。同时采用流式细胞仪在单个细胞水平上分析IFN-α诱导IFN-γ产生的细胞亚群以及该细胞亚群对肿瘤细胞的杀伤作用和信号传导机制。结果经IFN-α刺激后,PBMC能产生低剂量的IFN-γ。细胞亚群分析的结果表明,IFN-α诱导CD56+NK细胞产生IFN-γ,但对CD4+T和CD8+T细胞无明显作用。IFN-α促进NK细胞的杀伤功能。促进STAT1和STAT4磷酸化。结论 IFN-α通过磷酸化STAT1和STAT4,增加NK细胞IFN-γ分泌和增强杀伤功能。
Objective To investigate the effects of IFN-α on cytokine secretion, cytotoxicity and intracellular signaling in CD56 + NK cells. Methods PBMC from healthy volunteers were cultured with culture medium, IFN-α and IL-12 respectively. The level of IFN-γ in culture supernatant was detected by enzyme-linked immunosorbent assay (ELISA). At the same time using flow cytometry at the level of individual cells IFN-α-induced IFN-γ-induced cell subsets and the cell subsets on tumor cell killing and signaling mechanisms. Results After stimulation with IFN-α, PBMC could produce a low dose of IFN-γ. The results of cell subsets analysis showed that IFN-αinduced CD56 + NK cells to produce IFN-γ, but had no significant effect on CD4 + T and CD8 + T cells. IFN-alpha promotes NK cell killing function. Promotes phosphorylation of STAT1 and STAT4. Conclusion IFN-α can increase IFN-γ secretion and enhance cytotoxicity of NK cells by phosphorylating STAT1 and STAT4.