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Consequently, surrounding cells including immune cells in the tumor microenvironment (TME) are exposed to hypoglycemic, hypoxic, and low pH circumstances. Since effector T cells depend on the glycolysis for their survival and functions, the metabolically harsh TME established by cancer cells is unfavorable, resulting in the impairment of effective antitumor immune responses. By contrast, immunosuppressive cells such as regulatory T (Treg) cells can infiltrate, proliferate, survive, and exert immunosuppressive functions in the metabolically harsh TME, indicating the different metabolic dependance between effector T cells and Treg cells. Indeed, some metabolites that are harmful for effector T cells can be utilized by Treg cells; lactic acid, a harmful metabolite for effector T cells, is available for Treg cell proliferation and functions. Deficiency of amino acids such as tryptophan and glutamine in the TME impairs effector T cell activation but increases Treg cell populations. Furthermore, hypoxia upregulates fatty acid oxidation via hypoxia-inducible factor 1\u03b1 (HIF-1\u03b1) and promotes Treg cell migration. Adenosine is induced by the ectonucleotidases CD39 and CD73, which are strongly induced by HIF-1\u03b1, and reportedly accelerates Treg cell development by upregulating Foxp3 expression in T cells via A2AR-mediated signals. Therefore, this review focuses on the current views of the unique metabolism of Treg cells dictated by cancer cells. In addition, potential cancer combination therapies with immunotherapy and metabolic molecularly targeted reagents that modulate Treg cells in the TME are discussed to develop \u201cimmune metabolism-based precision medicine\u201d.<\/jats:p>","DOI":"10.1093\/intimm\/dxad035","type":"journal-article","created":{"date-parts":[[2023,10,13]],"date-time":"2023-10-13T00:15:56Z","timestamp":1697156156000},"page":"75-86","source":"Crossref","is-referenced-by-count":38,"title":["Metabolic advantages of regulatory T cells dictated by cancer cells"],"prefix":"10.1093","volume":"36","author":[{"given":"Masaki","family":"Kondo","sequence":"first","affiliation":[{"name":"Division of Cancer Immunology, Research Institute, National Cancer Center , Tokyo 104-0045 , Japan"},{"name":"Division of Cancer Immunology, Exploratory Oncology Research and Clinical Trial Center (EPOC), National Cancer Center , Chiba 277-8577 , Japan"},{"name":"Department of Neurosurgery, Nagoya University Graduate School of Medicine , Nagoya 466 \u2013 8550 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shogo","family":"Kumagai","sequence":"additional","affiliation":[{"name":"Division of Cancer Immunology, Research Institute, National Cancer Center , Tokyo 104-0045 , Japan"},{"name":"Division of Cancer Immunology, Exploratory Oncology Research and Clinical Trial Center (EPOC), National Cancer Center , Chiba 277-8577 , Japan"},{"name":"Division of Cellular Signaling, National Cancer Center Research Institute , Tokyo 104-0045 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyoshi","family":"Nishikawa","sequence":"additional","affiliation":[{"name":"Division of Cancer Immunology, Research Institute, National Cancer Center , Tokyo 104-0045 , Japan"},{"name":"Division of Cancer Immunology, Exploratory Oncology Research and Clinical Trial Center (EPOC), National Cancer Center , Chiba 277-8577 , Japan"},{"name":"Department of Immunology, Nagoya University Graduate School of Medicine , Nagoya 466 \u2013 8550 , Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,10,14]]},"reference":[{"key":"2024021623325590000_CIT0001","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1038\/s41568-019-0222-9","article-title":"How the ageing microenvironment influences tumour progression","volume":"20","author":"Fane","year":"2020","journal-title":"Nat Rev Cancer"},{"key":"2024021623325590000_CIT0002","doi-asserted-by":"crossref","first-page":"1565","DOI":"10.1126\/science.1203486","article-title":"Cancer immunoediting: integrating immunity\u2019s roles in cancer suppression and promotion","volume":"331","author":"Schreiber","year":"2011","journal-title":"Science"},{"key":"2024021623325590000_CIT0003","doi-asserted-by":"crossref","first-page":"834","DOI":"10.1038\/nrc2256","article-title":"Models, mechanisms and clinical evidence for cancer dormancy","volume":"7","author":"Aguirre-Ghiso","year":"2007","journal-title":"Nat Rev Cancer"},{"key":"2024021623325590000_CIT0004","doi-asserted-by":"crossref","first-page":"999","DOI":"10.1038\/ni1102-999","article-title":"Natural selection of tumor variants in the generation of \u201ctumor escape\u201d phenotypes","volume":"3","author":"Khong","year":"2002","journal-title":"Nat Immunol"},{"key":"2024021623325590000_CIT0005","doi-asserted-by":"crossref","first-page":"450","DOI":"10.1016\/j.ccell.2015.03.001","article-title":"Immune checkpoint blockade: a common denominator approach to cancer therapy","volume":"27","author":"Topalian","year":"2015","journal-title":"Cancer Cell"},{"key":"2024021623325590000_CIT0006","doi-asserted-by":"crossref","first-page":"56","DOI":"10.1126\/science.aaa8172","article-title":"The future of immune checkpoint therapy","volume":"348","author":"Sharma","year":"2015","journal-title":"Science"},{"key":"2024021623325590000_CIT0007","doi-asserted-by":"crossref","first-page":"eabc6424","DOI":"10.1126\/sciimmunol.abc6424","article-title":"Highly immunogenic cancer cells require activation of the WNT pathway for immunological escape","volume":"6","author":"Takeuchi","year":"2021","journal-title":"Sci Immunol"},{"key":"2024021623325590000_CIT0008","doi-asserted-by":"crossref","first-page":"168","DOI":"10.1016\/j.canlet.2019.05.003","article-title":"Treg-mediated acquired resistance to immune checkpoint inhibitors","volume":"457","author":"Saleh","year":"2019","journal-title":"Cancer Lett"},{"key":"2024021623325590000_CIT0009","doi-asserted-by":"crossref","first-page":"1151","DOI":"10.4049\/jimmunol.155.3.1151","article-title":"Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor \u03b1-chains (CD25). 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