Jin Jiakang, Lin Jinti, Xu Ankai, Lou Jianan, Qian Chao, Li Xiumao, Wang Yitian, Yu Wei, Tao Huimin
Department of Orthopedics, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Orthopedics Research Institute of Zhejiang University, Hangzhou, China.
Front Oncol. 2021 Jul 27;11:722916. doi: 10.3389/fonc.2021.722916. eCollection 2021.
Tumor microenvironment (TME) formation is a major cause of immunosuppression. The TME consists of a considerable number of macrophages and stromal cells that have been identified in multiple tumor types. CCL2 is the strongest chemoattractant involved in macrophage recruitment and a powerful initiator of inflammation. Evidence indicates that CCL2 can attract other host cells in the TME and direct their differentiation in cooperation with other cytokines. Overall, CCL2 has an unfavorable effect on prognosis in tumor patients because of the accumulation of immunosuppressive cell subtypes. However, there is also evidence demonstrating that CCL2 enhances the anti-tumor capability of specific cell types such as inflammatory monocytes and neutrophils. The inflammation state of the tumor seems to have a bi-lateral role in tumor progression. Here, we review works focusing on the interactions between cancer cells and host cells, and on the biological role of CCL2 in these processes.
肿瘤微环境(TME)的形成是免疫抑制的主要原因。TME由在多种肿瘤类型中已被鉴定出的大量巨噬细胞和基质细胞组成。CCL2是参与巨噬细胞募集的最强趋化因子,也是炎症的有力启动因子。有证据表明,CCL2可以吸引TME中的其他宿主细胞,并与其他细胞因子协同引导它们的分化。总体而言,由于免疫抑制细胞亚型的积累,CCL2对肿瘤患者的预后有不利影响。然而,也有证据表明CCL2可增强特定细胞类型(如炎性单核细胞和中性粒细胞)的抗肿瘤能力。肿瘤的炎症状态似乎在肿瘤进展中具有双向作用。在此,我们综述了聚焦于癌细胞与宿主细胞之间相互作用以及CCL2在这些过程中的生物学作用的研究。