Crosstalk Between the Tumor Microenvironment and Cancer Cells: A Promising Predictive Biomarker for Immune Checkpoint Inhibitors

Li, Xiaoying; Yang, Yiren; Huang, Qian; Deng, Yu; Guo, Fukun; Wang, Gang; Liu, Ming

doi:10.3389/fcell.2021.738373

Cited by 20 publications

(11 citation statements)

References 175 publications

(200 reference statements)

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“…pDCs secrete IFN-α, which inhibits proliferation and motility of ECs and increases expression of anti-angiogenic cytokines and chemokines through Toll-like receptor (TLR) 7 or signaling (Indraccolo et al 2002 ; Asselin-Paturel and Trinchieri 2005 ; Kawai and Akira 2011 ). Within the TME, cytokines produced by DCs may induce the activation and proliferation of Treg cells (Li et al 2021 ). A novel subset of tolerogenic DCs can also promote the differentiation of Treg cells through producing high levels of IL-10 (Gregori et al 2010 ).…”

Section: Tumor-suppressing Immune Cellsmentioning

confidence: 99%

Crosstalk between angiogenesis and immune regulation in the tumor microenvironment

Kim

Lee

2022

Arch. Pharm. Res.

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Cancer creates a complex tumor microenvironment (TME) composed of immune cells, stromal cells, blood vessels, and various other cellular and extracellular elements. It is essential for the development of anti-cancer combination therapies to understand and overcome this high heterogeneity and complexity as well as the dynamic interactions between them within the TME. Recent treatment strategies incorporating immune-checkpoint inhibitors and anti-angiogenic agents have brought many changes and advances in clinical cancer treatment. However, there are still challenges for immune suppressive tumors, which are characterized by a lack of T cell infiltration and treatment resistance. In this review, we will investigate the crosstalk between immunity and angiogenesis in the TME. In addition, we will look at strategies designed to enhance anti-cancer immunity, to convert “immune suppressive tumors” into “immune activating tumors,” and the mechanisms by which these strategies enhance effector immune cell infiltration.

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Section: Tumor-suppressing Immune Cellsmentioning

confidence: 99%

Crosstalk between angiogenesis and immune regulation in the tumor microenvironment

Kim

Lee

2022

Arch. Pharm. Res.

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“…The infiltration of the TME by immune cells is considered a key factor in cancer prognosis for many tumor types [ 4 , 5 , 6 , 7 ]. Activating immune cells such as cytotoxic T cells (CTLs) or Natural Killer (NK) cells has predominantly anti-tumor effects and is associated with overall improved clinical outcomes, e.g., by determining responsiveness to checkpoint inhibitor therapies when found within the tumor [ 8 , 9 , 10 , 11 ]. However, immunosuppressive immune cells such as regulatory T cells (T regs), myeloid-derived suppressor cells (MDSC), tumor-associated macrophages (TAM) and tumor-associated neutrophils (TAN) act in a pro-tumorigenic way and efficiently suppress the anti-tumor immune responses by diverse means [ 8 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Efficient Redirection of NK Cells by Genetic Modification with Chemokine Receptors CCR4 and CCR2B

Feigl

Stahringer

Peindl

et al. 2023

IJMS

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Natural killer (NK) cells are a subset of lymphocytes that offer great potential for cancer immunotherapy due to their natural anti-tumor activity and the possibility to safely transplant cells from healthy donors to patients in a clinical setting. However, the efficacy of cell-based immunotherapies using both T and NK cells is often limited by a poor infiltration of immune cells into solid tumors. Importantly, regulatory immune cell subsets are frequently recruited to tumor sites. In this study, we overexpressed two chemokine receptors, CCR4 and CCR2B, that are naturally found on T regulatory cells and tumor-resident monocytes, respectively, on NK cells. Using the NK cell line NK-92 as well as primary NK cells from peripheral blood, we show that genetically engineered NK cells can be efficiently redirected using chemokine receptors from different immune cell lineages and migrate towards chemokines such as CCL22 or CCL2, without impairing the natural effector functions. This approach has the potential to enhance the therapeutic effect of immunotherapies in solid tumors by directing genetically engineered donor NK cells to tumor sites. As a future therapeutic option, the natural anti-tumor activity of NK cells at the tumor sites can be increased by co-expression of chemokine receptors with chimeric antigen receptors (CAR) or T cell receptors (TCR) on NK cells can be performed in the future.

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“…In this scheme, players are not simply dysfunctional in TME, but also actively suppress other immune cells and promote tumor cells, ranging from growth, invasion, metastasis to immune evasion ( 27 ). Members found to promote tumors are regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), M2 tumor-associated macrophages (TAMs), resident or derived from bone marrow/spleen, N2 tumor-associated neutrophils (TANs), cancer-associated fibroblasts (CAFs), tolerogenic dendritic cells (DCs) and more details are summarized in Table 1 ( 76 – 78 ). Once cells migrate into the TME, they are polarized or differentiated under the local condition, and in return, these cells accelerate the immune-suppressive and tumor-promoting environment ( 37 ).…”

Section: Cellular Componentmentioning

confidence: 99%

A brief glimpse of a tangled web in a small world: Tumor microenvironment

Talaat

Kim²

2022

Front. Med.

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A tumor is a result of stepwise accumulation of genetic and epigenetic alterations. This notion has deepened the understanding of cancer biology and has introduced the era of targeted therapies. On the other hand, there have been a series of attempts of using the immune system to treat tumors, dating back to ancient history, to sporadic reports of inflamed tumors undergoing spontaneous regression. This was succeeded by modern immunotherapies and immune checkpoint inhibitors. The recent breakthrough has broadened the sight to other players within tumor tissue. Tumor microenvironment is a niche or a system orchestrating reciprocal and dynamic interaction of various types of cells including tumor cells and non-cellular components. The output of this complex communication dictates the functions of the constituent elements present within it. More complicated factors are biochemical and biophysical settings unique to TME. This mini review provides a brief guide on a range of factors to consider in the TME research.

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Crosstalk Between the Tumor Microenvironment and Cancer Cells: A Promising Predictive Biomarker for Immune Checkpoint Inhibitors

Cited by 20 publications

References 175 publications

Crosstalk between angiogenesis and immune regulation in the tumor microenvironment

Crosstalk between angiogenesis and immune regulation in the tumor microenvironment

Efficient Redirection of NK Cells by Genetic Modification with Chemokine Receptors CCR4 and CCR2B

A brief glimpse of a tangled web in a small world: Tumor microenvironment

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