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首页> 外文期刊>Oncology letters >Inflammation promotes oral squamous carcinoma immune evasion via induced programmed death ligand-1 surface expression
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Inflammation promotes oral squamous carcinoma immune evasion via induced programmed death ligand-1 surface expression

机译：炎症通过诱导程序性死亡配体1表面表达促进口腔鳞癌免疫逃逸

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摘要

The association between inflammation and cancer provides a new target for tumor biotherapy. The inflammatory cells and molecules within the tumor microenvironment have decisive dual roles in antitumor immunity and immune evasion. In the present study, phytohemagglutinin (PHA) was used to stimulate peripheral blood mononuclear cells (PBMCs) to simulate the tumor inflammatory microenvironment. The effect of immune cells and inflammatory cytokines on the surface expression of programmed cell death-1 ligand 1 (PD-L1) and tumor immune evasion was investigated using flow cytometry (FCM) and an in vivo xenotransplantation model. Based on the data, PHA-activated, but not resting, immune cells were able to promote the surface expression of PD-L1 in Tca8113 oral squamous carcinoma cells via the secretion of inflammatory cytokines, but not by cell-cell contact. The majority of the inflammatory cytokines had no significant effect on the proliferation, cell cycle progression and apoptosis of the Tca8113 cells, although they each induced the expression of PD-L1 in a dose-dependent manner. In total, 99% of the Tca8113 cells expressed PD-L1 following treatment with the supernatant of PHA-stimulated PBMCs. The PHA-supernatant pretreated Tca8113 cells unusually induced Tca8113 antigen-specific CD8(+) T cell apoptosis in vitro and the evasion of antigen-specific T cell attraction in a nude mouse tumor-bearing model. These results indicate a new mechanism for the promotion of tumor immune evasion by the tumor inflammatory microenvironment
机译：炎症和癌症之间的联系为肿瘤生物疗法提供了新的靶标。肿瘤微环境中的炎症细胞和分子在抗肿瘤免疫和免疫逃避中起决定性双重作用。在本研究中，植物血凝素（PHA）被用于刺激外周血单个核细胞（PBMC）以模拟肿瘤的炎症微环境。使用流式细胞仪（FCM）和体内异种移植模型研究了免疫细胞和炎性细胞因子对程序性细胞死亡1配体1（PD-L1）表面表达和肿瘤免疫逃逸的影响。根据这些数据，PHA激活但不静止的免疫细胞能够通过分泌炎性细胞因子来促进Tca8113口腔鳞状细胞中PD-L1的表面表达，但不能通过细胞接触来促进。尽管大多数炎症细胞因子均以剂量依赖的方式诱导PD-L1的表达，但它们对Tca8113细胞的增殖，细胞周期进程和凋亡均无明显影响。在用PHA刺激的PBMC的上清液处理后，总共有99％的Tca8113细胞表达PD-L1。 PHA上清液预处理的Tca8113细胞在体外异常诱导Tca8113抗原特异性CD8（+）T细胞凋亡，并逃避了裸鼠荷瘤模型中抗原特异性T细胞的吸引。这些结果表明通过肿瘤炎性微环境促进肿瘤免疫逃逸的新机制。

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