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Metabolism of Dendritic Cells in Tumor Microenvironment: For Immunotherapy

Journal

FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.613492

Keywords

dendritic cells; tumor microenvironment; metabolism; glucose; amino acid; lipid; therapy

Categories

Funding

  1. National Natural Science Foundation of China [82073097, 81874139, 81672991, 82072594, 81672787]
  2. Shenzhen Science and Technology Program [KQTD20170810160226082]
  3. Shenzhen Municipal Government of China [JCYJ20180507184647104]
  4. Hunan Provincial Key Area RD Program [2019SK2253]

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Dendritic cells (DCs) play a crucial role in capturing antigens from pathogens or tumors and presenting them to T cells for immune response. However, the immune activity of DCs is generally inhibited in the tumor microenvironment (TME) due to abnormal metabolism of tumor cells causing metabolic changes in TME, limiting the function of DCs and leading to tumor immune escape.
Dendritic cells (DCs) are a type of an antigen-presenting cell which undertake a job on capturing antigens coming from pathogens or tumors and presenting to T cells for immune response. The metabolism of DCs controls its development, polarization, and maturation processes and provides energy support for its functions. However, the immune activity of DCs in tumor microenvironment (TME) is inhibited generally. Abnormal metabolism of tumor cells causes metabolic changes in TME, such as hyperglycolysis, lactate and lipid accumulation, acidification, tryptophan deprivation, which limit the function of DCs and lead to the occurrence of tumor immune escape. Combined metabolic regulation with immunotherapy can strengthen the ability of antigen-presentation and T cell activation of DCs, improve the existing anti-tumor therapy, and overcome the defects of DC-related therapies in the current stage, which has great potential in oncology therapy. Therefore, we reviewed the glucose, lipid, and amino acid metabolism of DCs, as well as the metabolic changes after being affected by TME. Together with the potential metabolic targets of DCs, possible anti-tumor therapeutic pathways were summarized.

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