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Cancer Stem Cells: Emerging Key Players in Immune Evasion of Cancers

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.692940

关键词

cancer; cancer stem cells; immune cells; tumor microenvironment; immune evasion

资金

  1. RGC General Research Fund [15102020]
  2. Collaborative Research Fund [C7026-18G]
  3. Health and Medical Research Fund [05161216]
  4. Research Impact Fund [R5050-18F]

向作者/读者索取更多资源

Immune cells play a crucial role in driving cancer cells towards stemness and enabling cancer stem cells to evade immune surveillance by affecting various immune cells in the tumor microenvironment. Targeting CSCs with immunotherapy disrupts the interaction between immune cells and CSCs, offering a novel strategy against cancer.
Cancer stem cells (CSCs) are subpopulations of undifferentiated cancer cells within the tumor bulk that are responsible for tumor initiation, recurrence and therapeutic resistance. The enhanced ability of CSCs to give rise to new tumors suggests potential roles of these cells in the evasion of immune surveillance. A growing body of evidence has described the interplay between CSCs and immune cells within the tumor microenvironment (TME). Recent data have shown the pivotal role of some major immune cells in driving the expansion of CSCs, which concurrently elicit evasion of the detection and destruction of various immune cells through a number of distinct mechanisms. Here, we will discuss the role of immune cells in driving the stemness of cancer cells and provide evidence of how CSCs evade immune surveillance by exerting their effects on tumor-associated macrophages (TAMs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), T-regulatory (Treg) cells, natural killer (NK) cells, and tumor-infiltrating lymphocytes (TILs). The knowledge gained from the interaction between CSCs and various immune cells will provide insight into the mechanisms by which tumors evade immune surveillance. In conclusion, CSC-targeted immunotherapy emerges as a novel immunotherapy strategy against cancer by disrupting the interaction between immune cells and CSCs in the TME.

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