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. 2021 Aug 19;19(3):370–383. doi: 10.1038/s41423-021-00753-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Metabolic regulation of DC function within the TME. DC metabolism is tightly linked with immune function and may be dysregulated within the TME in several ways. Competition between DCs and tumor cells for limiting resources can result in a lack of nutrient support for metabolic pathways essential to DC activation and maturation. Immunosuppressive cytokines, enzymes, and lipid bodies derived from tumors and tumor-associated cells can all alter metabolic pathways that support antitumor DC function while also driving alternative pathways associated with immune tolerance, including driving the differentiation of tumor-supporting Tregs. Immunosuppressive metabolites (adenosine, lactate, gangliosides and IDO generated by tumor cells) may trigger a shift in DCs from antitumor to protumor functionality. Abbreviations in this figure not defined in the main body of the text: PKM2, pyruvate kinase M2; A2R/A2b, A2 adenosine receptor. MCT, monocarboxylate transporters