期刊
FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.754196
关键词
myeloid-derived suppressor cells (MDSCs); immune checkpoint blockade (ICB) therapy; immunosuppression; programmed cell death protein 1 (PD-1); the tumor microenvironment (TME)
类别
资金
- National Natural Science Foundation for Key Programs of China [81774261]
- Project of Administration of Traditional Chinese Medicine of Guangdong Province of China [20191007]
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that are activated under pathological conditions, such as cancer, or mature myeloid cells that are converted into immune-suppressive cells via tumor-derived exosomes. They play a potent role in supporting tumor processes through various mechanisms, including inducing immune checkpoint blockade therapy resistance and promoting tumor progression. Targeting MDSCs is considered a potential therapeutic strategy to enhance the antitumor efficacy of immune checkpoint blockade therapy in multiple cancer cases.
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that are activated under pathological conditions, such as cancer, or mature myeloid cells that are converted immune-suppressive cells via tumor-derived exosomes, and potently support the tumor processes at different levels. Currently, multiple studies have demonstrated that MDSCs induce immune checkpoint blockade (ICB) therapy resistance through their contribution to the immunosuppressive network in the tumor microenvironment. In addition, non-immunosuppressive mechanisms of MDSCs such as promotion of angiogenesis and induction of cancer stem cells also exert a powerful role in tumor progression. Thus, MDSCs are potential therapeutic targets to enhance the antitumor efficacy of ICB therapy in cases of multiple cancers. This review focuses on the tumor-promoting mechanism of MDSCs and provides an overview of current strategies that target MDSCs with the objective of enhancing the antitumor efficacy of ICB therapy.
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