CCL4 Signaling in the Tumor Microenvironment
CCL4 Signaling in the Tumor Microenvironment
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DOI：
10.1007/978-3-030-36667-4_3
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发表时间：
2020-01-01
期刊：
影响因子：
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通讯作者：
Baba, Tomohisa
中科院分区：
文献类型：
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作者：
Mukaida, Naofumi;Sasaki, So-ichiro;Baba, Tomohisa
CCL 4是一种CC趋化因子，以前称为巨噬细胞炎性蛋白（MIP）-1 β，通过与其特异性受体CCR 5的相互作用，与相关但不同的CC趋化因子如CCL 3和CCL 5（也可以结合CCR 5）合作，对各种类型的免疫和非免疫细胞具有不同的作用。一些证据表明，CCL 4可以通过募集调节性T细胞和促肿瘤发生的巨噬细胞，并作用于肿瘤微环境中存在的其他驻留细胞，如成纤维细胞和内皮细胞，以促进其促肿瘤发生的能力，从而促进肿瘤的发展和进展。这些观察结果表明CCR 5拮抗剂用于癌症治疗的潜在功效。相反，在某些情况下，CCL 4可以通过募集具有吞噬能力的溶细胞淋巴细胞和巨噬细胞来增强肿瘤免疫。因此，目前，CCR 5拮抗剂的临床应用需要更详细地分析CCL 4和其他CCR 5结合趋化因子在肿瘤微环境中的作用。
CCL4, a CC chemokine, previously known as macrophage inflammatory protein (MIP)-1 beta, has diverse effects on various types of immune and nonimmune cells by the virtue of its interaction with its specific receptor, CCR5, in collaboration with related but distinct CC chemokines such as CCL3 and CCL5, which can also bind CCR5. Several lines of evidence indicate that CCL4 can promote tumor development and progression by recruiting regulatory T cells and pro-tumorigenic macrophages, and acting on other resident cells present in the tumor microenvironment, such as fibroblasts and endothelial cells, to facilitate their pro-tumorigenic capacities. These observations suggest the potential efficacy of CCR5 antagonists for cancer treatment. On the contrary, under some situations, CCL4 can enhance tumor immunity by recruiting cytolytic lymphocytes and macrophages with phagocytic ability. Thus, presently, the clinical application of CCR5 antagonists warrants more detailed analysis of the role of CCL4 and other CCR5-binding chemokines in the tumor microenvironment.