Department of Medicine, Karolinska Institutet (KI), Solna, Sweden.
Cell Therapy Institute, Nova Southeastern University, Fort Lauderdale, FL, United States.
Front Immunol. 2018 Sep 25;9:2159. doi: 10.3389/fimmu.2018.02159. eCollection 2018.
Chemokines govern leukocyte migration by attracting cells that express their cognate ligands. Many cancer types show altered chemokine secretion profiles, favoring the recruitment of pro-tumorigenic immune cells and preventing the accumulation of anti-tumorigenic effector cells. This can ultimately result in cancer immune evasion. The manipulation of chemokine and chemokine-receptor signaling can reshape the immunological phenotypes within the tumor microenvironment in order to increase the therapeutic efficacy of cancer immunotherapy. Here we discuss the three chemokine-chemokine receptor axes, CXCR1/2-CXCL1-3/5-8, CXCR3-CXCL9/10/11, and CXCR4-CXCL12 and their role on pro-tumorigenic immune cells and anti-tumorigenic effector cells in solid tumors. In particular, we summarize current strategies to target these axes and discuss their potential use in treatment approaches.
趋化因子通过吸引表达其同源配体的细胞来控制白细胞的迁移。许多癌症类型表现出改变的趋化因子分泌谱，有利于促进肿瘤发生的免疫细胞的募集，并防止抗肿瘤效应细胞的积累。这最终可能导致癌症免疫逃逸。趋化因子和趋化因子受体信号的操纵可以重塑肿瘤微环境中的免疫表型，以提高癌症免疫治疗的疗效。在这里，我们讨论了三个趋化因子-趋化因子受体轴，CXCR1/2-CXCL1-3/5-8、CXCR3-CXCL9/10/11 和 CXCR4-CXCL12 以及它们在实体瘤中对促肿瘤免疫细胞和抗肿瘤效应细胞的作用。特别是，我们总结了目前靶向这些轴的策略，并讨论了它们在治疗方法中的潜在用途。
