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卢礼兵, 陈娇, 冯云, 等. 炎症细胞因子诱导Tca8113细胞表达PD-L1的作用研究[J]. 四川大学学报(医学版), 2013, 44(1): 42-45.
引用本文: 卢礼兵, 陈娇, 冯云, 等. 炎症细胞因子诱导Tca8113细胞表达PD-L1的作用研究[J]. 四川大学学报(医学版), 2013, 44(1): 42-45.
LU Li-bing, CHEN Jiao, FENG Yun, et al. Inflammatory Factors Promote the Expression of PD-L1 in Tca8113[J]. Journal of Sichuan University (Medical Sciences), 2013, 44(1): 42-45.
Citation: LU Li-bing, CHEN Jiao, FENG Yun, et al. Inflammatory Factors Promote the Expression of PD-L1 in Tca8113[J]. Journal of Sichuan University (Medical Sciences), 2013, 44(1): 42-45.

炎症细胞因子诱导Tca8113细胞表达PD-L1的作用研究

Inflammatory Factors Promote the Expression of PD-L1 in Tca8113

  • 摘要: 目的 通过研究炎症细胞因子对人舌鳞状细胞癌细胞Tca8113中程序性死亡因子配体-1(programmed death 1 ligand-1,PD-L1)的表达的影响,探讨肿瘤炎性微环境在肿瘤细胞免疫逃逸中的作用和机制。 方法 用流式细胞分析术(FCM)检测Tca8113在各种炎症细胞因子白介素(IL)-1β、IL-2、IL-6、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)以及其他诱导条件牙龈卟啉单胞菌代谢产物(Pg-sup)及活化外周血单个核细胞的代谢产物(PHA-sup)处理下PD-L1的表达变化。 结果 PHA-sup、Pg-sup液,IL-1β、IL-6、TNF-α、IFN-γ等炎症相关细胞因子均能诱导Tca8113中PD-L1的表达,与未做处理的Tca8113(对照组)比较差异有统计学意义(P<0.05), 但IL-2诱导后PD-L1的表达与对照组的差异无统计学意义(P>0.05)。与单个炎症细胞因子诱导比较,炎症细胞因子组合诱导的PD-L1表达均有增高(P<0.05),炎症细胞因子在诱导PD-L1表达中相互之间存在协同效应,其中,IL-1β+IFN-γ、TNF-α+IFN-γ以及L-1β+IL-6+IFN-γ+TNF-α这3组的表达量高于其他各组(P<0.05)。 结论 肿瘤微环境炎症细胞因子促进肿瘤细胞表达PD-L1,在肿瘤免疫逃逸中发挥重要作用。

     

    Abstract: Objective To investigate the mechanism of immunologic escape in the tumor microenvironment, study the expression of programmed death 1 ligand-1 (PD-L1) in Tca8113 with treatment of inflammatory factors. Methods The expression of PD-L1 treated with inflammatory factors (IL-1β, IL-2, IL-6, TNF-α, IFN-γ) was detected by flow cytometry (FCM). Results The expression of PD-L1 in Tca8113 was up-regulated conspicuously with treatment of inflammatory factors (P<0.05), including:IL-1β, IL-6, TNF-α, IFN-γ. And the factors played the role in synergistic effects, most significantly in the groups of IL-1β+IFN-γ, TNF-α+IFN-γ and IL-1β+IL-6+IFN-γ+TNF-α. But the influence of IL-2 on the expression of PD-L1 was not significant (P>0.05). Conclusion With the up-regulated expression of PD-L1, the tumor would be escaped more easily from the immunoreactions, while there were an abundance of inflammatory factors in the tumor microenvironment.

     

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