肿瘤微环境
趋化因子
CCL5
趋化因子受体
三氯化碳
癌症研究
巨噬细胞
趋化因子受体CCR5
生物
免疫学
免疫系统
化学
细胞生物学
四氯化碳
T细胞
四氯化碳
体外
白细胞介素2受体
生物化学
有机化学
四氯化碳
作者
Naofumi Mukaida,Soichiro Sasaki,Tomohisa Baba
标识
DOI:10.1007/978-3-030-36667-4_3
摘要
CCL4, a CC chemokine, previously known as macrophage inflammatory protein (MIP)-1β, 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.
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