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Abstract
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.
Highlights
Immune evasion is a hallmark of carcinogenesis [1]
We focus on the impact of the CXCR1/2, CXCR3, and CXCR4 chemokine axes on recruitment of pro-tumorigenic and anti-tumorigenic immune cells in solid malignancies
We recently showed that CXCR2 expression is downregulated on tumor-infiltrating NK cells in renal cell carcinoma (RCC) and genetic modification to re-express CXCR2 enhanced recruitment of NK cells to the tumor site [39]
Summary
Immune evasion is a hallmark of carcinogenesis [1]. Tumor cells interact closely with stromal cells, immune cells and the extracellular matrix (ECM). In genetically modified mice that expressed human CXCL8, MDSC were efficiently recruited to the tumor site and suppressed T cell activity [22]. - Targeting CXCR2 in Snail+ ovarian cancer xenograft models inhibits MDSC recruitment and prolongs overall survival of tumor-bearing mice
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