CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment
CCL2: важный медиатор взаимодействия между опухолевыми клетками и клетками организма в микроокружении опухоли
2021-07-27
SCID: 54.1/ne4gwt44
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CCL2immunosuppressioninflammatory monocytesmacrophage recruitmenttumor microenvironment
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Abstract (AI)
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.
Key Findings
1
CCL2 can also enhance antitumor activity in specific populations, including inflammatory monocytes and neutrophils.
2
CCL2 cooperates with other cytokines to direct the differentiation of recruited host cells within tumors.
3
CCL2 generally worsens cancer prognosis by promoting accumulation of immunosuppressive cell subtypes.
4
CCL2 is a major chemoattractant that recruits macrophages and other host cells into the tumor microenvironment.
5
Tumor-associated inflammation has bidirectional effects, potentially either promoting or restraining tumor progression.
Research Object
CCL2-mediated interactions between tumor cells and host cells in the tumor microenvironment
Research Subject
The role of CCL2 in recruiting and differentiating tumor-microenvironment host cells and modulating tumor inflammation, immunosuppression, and anti-tumor responses
Publication Details
Publication Date
2021-07-27
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