Novel Characterization of Myeloid-Derived Suppressor Cells in Tumor Microenvironment

Li, Yanan; He, Hongdan; Jihu, Ribu; Zhou, Junfu; Zeng, Rui; Yan, Heng-Xiu

doi:10.3389/fcell.2021.698532

Cited by 17 publications

(9 citation statements)

References 152 publications

(164 reference statements)

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“…[ 36 , 37 ] In an extensive series of experiments using tumor‐bearing mice and PBMCs from cancer patients, we have identified TAMos as an ACT enhancer that promotes T CM cell differentiation. In contrast to the previously reported immunosuppressive functions of monocytes, which primarily hamper immune responses and promote tumor progression, [ 38 ] our findings reveal an unexpected beneficial antitumor aspect of this immune cell type, thus providing a deeper understanding of the multiple and complex functions of monocytes.…”

Section: Discussioncontrasting

confidence: 90%

Tumor‐Associated Monocytes Reprogram CD8⁺ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

Yang,

Liu,

Zhu

et al. 2024

Advanced Science

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CD8+ T cells are critical for host antitumor responses, whereas persistent antigenic stimulation and excessive inflammatory signals lead to T cell dysfunction or exhaustion. Increasing early memory T cells can improve T cell persistence and empower T cell‐mediated tumor eradication, especially for adoptive cancer immunotherapy. Here, it is reported that tumor‐associated monocytes (TAMos) are highly correlated with the accumulation of CD8+ memory T cells in human cancers. Further analysis identifies that TAMos selectively reprogram CD8+ T cells into T central memory‐like (TCM‐like) cells with enhanced recall responses. L‐NMMA, a pan nitric oxide synthase inhibitor, can mitigate TAMo‐mediated inhibition of T cell proliferation without affecting TCM‐like cell generation. Moreover, the modified T cells by TAMo exposure and L‐NMMA treatment exhibit long‐term persistence and elicit superior antitumor effects in vivo. Mechanistically, the transmembrane protein CD300LG is involved in TAMo‐mediated TCM‐like cell polarization in a cell‐cell contact‐dependent manner. Thus, the terminally differentiated TAMo subset (CD300LGhighACElow) mainly contributes to TCM‐like cell development. Taken together, these findings establish the significance of TAMos in boosting T‐cell antitumor immunity.

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Section: Discussioncontrasting

confidence: 90%

Tumor‐Associated Monocytes Reprogram CD8⁺ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

Yang,

Liu,

Zhu

et al. 2024

Advanced Science

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“…The second reason for therapies inefficacy or failure is the tumor microenvironment (TME) that protects tumor cells from both innate and adaptive immunity attack. TME is generated by myeloid-derived suppressor cells (MDSCs) that are a small subpopulation of the low differentiated monocytes involved with the physiological regulation of the immune response during pregnancy and cancer [5,6]. MDSCs contribute to maternal-fetal tolerance or suppressing the immune attack to cancer cells [7].…”

Section: Discussionmentioning

confidence: 99%

The Perfect Combination of the Most Powerful Cancer Immunotherapy with the Best Targeted Chemotherapy

Pak¹

2022

CTOIJ

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Cancer is one of the leading causes of death globally. There are cancer treatments like chemotherapy, radiotherapy, surgery, and immunotherapy. A combination of therapies can lead to a cancer cure. Myeloid-derived suppressor cells (MDSCs) activity prevents the success of many immune-and chemotherapies. MDSCs depletion prevails over other cancer immunotherapies because it activates both innate and adaptive immunity. On the other hand, the best-targeted chemotherapy specifically kills cancer cells, including cancer stem ones that are at the roots of metastases leading to 90% of deaths of cancer. The low differentiated MDSCs, cancer stem cells, and most cancers absorb alpha-fetoprotein (AFP) loaded with nutrients through AFP receptor (AFPR)-mediated endocytosis. So, the AFP-toxin drug is targeted chemotherapy that hits simultaneously to MDSCs and cancer cells. In my opinion, it is the perfect combination of the most powerful cancer immunotherapy and the best-targeted chemotherapy. For example, the AFP-maytansine conjugate demonstrated 100% survival in tumor-bearing T cell-deficient mice.

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“…MDSCs exhibit low expression of Human Leukocyte Antigen–DR isotype (HLA-DR) and CD14, the cell surface receptors essential for proper immune responses to antigens, resulting in an immune response defect ( 43 , 48 ). The activation and recruitment of MDSCs in the TME is mediated through increased production of specific chemokines, cytokines, and factors, including IL-4, IL-6, IL-10, IL-12, IL-13, CCL5, CCL2, CXCL2, CXCL5, CXCL12, vascular endothelial growth factor (VEGF)-A, transforming growth factor (TGF)-β, and granulocytic-colony stimulating factor (G-CSF) in TME ( 49 – 52 ). These molecules are critical in shaping the tumor microenvironment and promoting MDSC-mediated immune suppression.…”

Section: Breast Tmementioning

confidence: 99%

Cellular interactions in tumor microenvironment during breast cancer progression: new frontiers and implications for novel therapeutics

Akinsipe,

Mohamedelhassan,

Akinpelu

et al. 2024

Front. Immunol.

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The breast cancer tumor microenvironment (TME) is dynamic, with various immune and non-immune cells interacting to regulate tumor progression and anti-tumor immunity. It is now evident that the cells within the TME significantly contribute to breast cancer progression and resistance to various conventional and newly developed anti-tumor therapies. Both immune and non-immune cells in the TME play critical roles in tumor onset, uncontrolled proliferation, metastasis, immune evasion, and resistance to anti-tumor therapies. Consequently, molecular and cellular components of breast TME have emerged as promising therapeutic targets for developing novel treatments. The breast TME primarily comprises cancer cells, stromal cells, vasculature, and infiltrating immune cells. Currently, numerous clinical trials targeting specific TME components of breast cancer are underway. However, the complexity of the TME and its impact on the evasion of anti-tumor immunity necessitate further research to develop novel and improved breast cancer therapies. The multifaceted nature of breast TME cells arises from their phenotypic and functional plasticity, which endows them with both pro and anti-tumor roles during tumor progression. In this review, we discuss current understanding and recent advances in the pro and anti-tumoral functions of TME cells and their implications for developing safe and effective therapies to control breast cancer progress.

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Novel Characterization of Myeloid-Derived Suppressor Cells in Tumor Microenvironment

Cited by 17 publications

References 152 publications

Tumor‐Associated Monocytes Reprogram CD8⁺ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

Tumor‐Associated Monocytes Reprogram CD8⁺ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

The Perfect Combination of the Most Powerful Cancer Immunotherapy with the Best Targeted Chemotherapy

Cellular interactions in tumor microenvironment during breast cancer progression: new frontiers and implications for novel therapeutics

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Novel Characterization of Myeloid-Derived Suppressor Cells in Tumor Microenvironment

Cited by 17 publications

References 152 publications

Tumor‐Associated Monocytes Reprogram CD8+ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

Tumor‐Associated Monocytes Reprogram CD8+ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

The Perfect Combination of the Most Powerful Cancer Immunotherapy with the Best Targeted Chemotherapy

Cellular interactions in tumor microenvironment during breast cancer progression: new frontiers and implications for novel therapeutics

Contact Info

Product

Resources

About

Tumor‐Associated Monocytes Reprogram CD8⁺ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects

Tumor‐Associated Monocytes Reprogram CD8⁺ T Cells into Central Memory‐Like Cells with Potent Antitumor Effects