Department of Neurosurgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Clin Exp Immunol. 2020 Oct;202(1):47-59. doi: 10.1111/cei.13476. Epub 2020 Jun 30.
Recurrence and diffuse infiltration challenge traditional therapeutic strategies for malignant glioma. Immunotherapy appears to be a promising approach to obtain long-term survival. Dendritic cells (DCs), the most specialized and potent antigen-presenting cells (APCs), play an important part in initiating and amplifying both the innate and adaptive immune responses against cancer cells. However, cancer cells can escape from immune surveillance by inhibiting maturation of DCs. Until the present, molecular mechanisms of maturation inhibition of DCs in the tumor microenvironment (TME) have not been fully revealed. Our study showed that pretreatment with tumor-conditioned medium (TCM) collected from supernatant of primary glioma cells significantly suppressed the maturation of DCs. TCM pretreatment significantly changed the morphology of DCs, TCM decreased the expression levels of CD80, CD83, CD86 and interleukin (IL)-12p70, while it increased the expression levels of IL-10, transforming growth factor (TGF)-β and IL-6. RNA-Seq showed that TCM pretreatment significantly increased the gene expression level of suppressor of cytokine signaling 1 (SOCS1) in DCs. suppressor of cytokine signaling 1 (SOCS1) knock-down significantly antagonized the maturation inhibition of DCs by TCM, which was demonstrated by the restoration of maturation markers. TCM pretreatment also significantly suppressed T cell viability and T helper type 1 (Th1) response, and SOCS1 knock-down significantly antagonized this suppressive effect. Further, TCM pretreatment significantly suppressed p65 nuclear translocation and transcriptional activity in DCs, and SOCS1 knock-down significantly attenuated this suppressive effect. In conclusion, our research demonstrates that TCM up-regulate SOCS1 to suppress the maturation of DCs via the nuclear factor-kappa signaling pathway.
复发性和弥漫浸润性挑战了恶性神经胶质瘤的传统治疗策略。免疫疗法似乎是获得长期生存的一种很有前途的方法。树突状细胞(DCs)是最专业和最有效的抗原提呈细胞(APCs),在启动和放大针对癌细胞的固有和适应性免疫反应方面发挥着重要作用。然而,癌细胞可以通过抑制 DCs 的成熟来逃避免疫监视。直到目前为止,肿瘤微环境(TME)中 DCs 成熟抑制的分子机制尚未完全揭示。我们的研究表明,用从原代神经胶质瘤细胞上清液中收集的肿瘤条件培养基(TCM)预处理可显著抑制 DCs 的成熟。TCM 预处理显著改变了 DCs 的形态,降低了 CD80、CD83、CD86 和白细胞介素(IL)-12p70 的表达水平,而增加了 IL-10、转化生长因子(TGF)-β和 IL-6 的表达水平。RNA-Seq 显示,TCM 预处理显著增加了 DCs 中细胞因子信号转导抑制因子 1(SOCS1)的基因表达水平。SOCS1 敲低显著拮抗了 TCM 对 DCs 成熟的抑制作用,表现为成熟标志物的恢复。TCM 预处理还显著抑制了 T 细胞活力和辅助性 T 细胞 1(Th1)反应,而 SOCS1 敲低显著拮抗了这种抑制作用。此外,TCM 预处理显著抑制了 DCs 中 p65 核易位和转录活性,而 SOCS1 敲低显著减弱了这种抑制作用。总之,我们的研究表明,TCM 通过核因子-κB 信号通路上调 SOCS1 来抑制 DCs 的成熟。