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. 2023 May 19;14:1125874. doi: 10.3389/fimmu.2023.1125874

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Copyright © 2023 Kumar and Stewart

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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DCs in TIME and their immunometabolic reprogramming. TME or TIME-released chemokines induce DC chemotaxis. cDCs migrate to tumor DLNs for antigen presentation for adaptive immune cells (T and B cells) to induce antitumor immunity. However, IDO release from pDCs induces immunosuppression. Furthermore, adenosine in TME or TIME via A2bR blocks immunometabolic shift to glycolysis from OXPHOS and increases AMPK levels. Thus, tumor-associated DCs (TADCs) show an increased OXPHOS and FAO giving them an immunosuppressive phenotype to survive in the nutrient-deficient TME or TIME. These immunosuppressive TADCs release different factors and molecules to support immunosuppressive TIME, angiogenesis, and tumor growth and metastasis. Details are mentioned in the text.