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目的:探讨IL-12增强正常人NK细胞对Jurkat细胞杀伤功能的相关机制。方法:纯化正常人NK细胞,分为加或不加IL-12两个刺激组,通过基因芯片筛选差异基因,并通过流式细胞术在单个细胞水平检测相关杀伤分子的表达。结果:基因芯片系统结果显示IL-12刺激组和未刺激组相比,17种基因具有显著性差异(fold change≥10),其中5种基因上调,12种基因下调。在IL-12的刺激作用下,TRAIL的表达在CD56+CD16+和CD56-CD16+NK细胞上显著增加。同时,Jurkat细胞亦高表达TRAIL受体TRAIL-R2(DR5)。TRAIL中和抗体RIK-2可以阻断IL-12诱导的NK细胞对Jurkat细胞的杀伤功能。结论:TRAIL是IL-12增强正常人NK细胞对Jurkat细胞杀伤功能的主要途径之一。
Objective: To investigate the mechanism of interleukin-12 (IL-12) -mediated NK cell killing of Jurkat cells. Methods: The normal human NK cells were purified and divided into two groups with and without IL-12. The genes were screened by gene chip, and the expression of related killer molecules was detected by flow cytometry at the single cell level. Results: The results of gene chip system showed that 17 kinds of genes were significantly changed (fold change ≥10) in IL-12 stimulation group compared with unstimulated group, of which 5 genes were up-regulated and 12 genes were down-regulated. Under the stimulation of IL-12, TRAIL expression was significantly increased on CD56 + CD16 + and CD56-CD16 + NK cells. Meanwhile, Jurkat cells also overexpress TRAIL receptor TRAIL-R2 (DR5). The TRAIL neutralizing antibody RIK-2 blocked IL-12-induced NK cell killing of Jurkat cells. Conclusion: TRAIL is one of the main ways that IL-12 enhances the killing effect of NK cells on Jurkat cells.