2017
DOI: 10.1007/978-94-024-1170-6_5
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Immune Cell Metabolism in Tumor Microenvironment

Abstract: Tumor microenvironment (TME) is composed of tumor cells, immune cells, cytokines, extracellular matrix, etc. The immune system and the metabolisms of glucose, lipids, amino acids, and nucleotides are integrated in the tumorigenesis and development. Cancer cells and immune cells show metabolic reprogramming in the TME, which intimately links immune cell functions and edits tumor immunology. Recent findings in immune cell metabolism hold the promising possibilities toward clinical therapeutics for treating cance… Show more

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Cited by 28 publications
(22 citation statements)
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“…Differentiation and activation of pro-tumor immune cells, including myeloid-derived suppressor cells (MDSCs), M2 macrophages, regulatory T cells, and suppressing antitumor immune cells (CD8+ T cells, M1 macrophages, and N1 neutrophils) are promoted by the deprivation of nutrients [42]. Tumor-associated immune cells regulate their metabolism for survival, differentiation, and pro/antitumor functions by modulating several signaling pathways, such as PI3K-Akt, mTOR, HIF-1, and c-Myc [42]. Glycolytic metabolism activated by inflammation may be upregulated during the tumor-initiation process by HIF-1 activation in both cancer and immune cells.…”
Section: Metabolic Relationship Between Cancer Cells and Tumor-associmentioning
confidence: 99%
See 1 more Smart Citation
“…Differentiation and activation of pro-tumor immune cells, including myeloid-derived suppressor cells (MDSCs), M2 macrophages, regulatory T cells, and suppressing antitumor immune cells (CD8+ T cells, M1 macrophages, and N1 neutrophils) are promoted by the deprivation of nutrients [42]. Tumor-associated immune cells regulate their metabolism for survival, differentiation, and pro/antitumor functions by modulating several signaling pathways, such as PI3K-Akt, mTOR, HIF-1, and c-Myc [42]. Glycolytic metabolism activated by inflammation may be upregulated during the tumor-initiation process by HIF-1 activation in both cancer and immune cells.…”
Section: Metabolic Relationship Between Cancer Cells and Tumor-associmentioning
confidence: 99%
“…Glycolytic metabolism activated by inflammation may be upregulated during the tumor-initiation process by HIF-1 activation in both cancer and immune cells. Particularly, during tumor progression, HIF-1 up-regulation in tumor-associated macrophages (TAMs), tumor-associated dendritic cells (TADCs), MDSCs, and Tregs contributes to immune suppression and angiogenesis by PD-L1 expression, adenosine-adenosine receptor interaction, and lactate release that facilitate tumor growth [42].…”
Section: Metabolic Relationship Between Cancer Cells and Tumor-associmentioning
confidence: 99%
“…While some investigators have reported that mitochondrial ROS (mROS) stimulate macrophage expression of pro-inflammatory cytokines, other researchers have instead observed the induction of an anti-inflammatory phenotype; hence, further study is required to fully understand these events [99][100][101][102]. The glycolytic reprogramming of TAM is regulated by oxygen sensors including prolyl-hydroxylases (PHDs) and is accompanied by proton pumping and acidification of M2 macrophages that subsequently impair antitumor responses [103]. Similarly, while resting NK cells typically utilize OXPHOS, exposure to high doses of tissue damage-associated cytokine IL-15 stimulates conversion to glycolytic activity [104].…”
Section: Hypoxia Modifies the Resting Metabolic Status Of Immune Cellsmentioning
confidence: 99%
“…On the other hand, TME can reprogram the metabolism of an immune cell ( 16 ), reducing immune activation signals, downregulating antigen recognition and presentation, and making tumor cells escape from host immune surveillance ( 17 ), thus causing tumor immune escape. Early invasion of immune cells, such as macrophages, lymphocytes, natural killer (NK) cells, and DCs, is essential for anti-tumor immunity.…”
Section: Introductionmentioning
confidence: 99%