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. 2024 Dec 19;23:273. doi: 10.1186/s12943-024-02193-7

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 3 — Key metabolic pathways modulating Tregs functions in the tumor microenvironment of OSCC. The suppressive function of regulatory T cells (Tregs) in the tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC) is shaped by key metabolic pathways, including the CD39/CD73 adenosine axis (A), tryptophan (Trp)–kynurenine (Kyn)–aryl hydrocarbon receptor (AHR) pathway (B) and phosphatidylinositol 3‐kinase (PI3K) ‐protein kinase B (Akt)‐mammalian target of rapamycin (mTOR) Pathway (C). The CD39/CD73 cascade hydrolyzes ATP to adenosine, which enhances Treg suppressive functions and inhibits effector T cells. The Trp–Kyn–AHR pathway, mediated by indoleamine 2,3-dioxygenase 1 (IDO1), converts Trp to Kyn, activating AHR to promote Treg stability and immunosuppression. PI3K-Akt-mTOR signaling supports glucose uptake, glycolysis, and lipid metabolism to adapt to the nutrient-deprived TME. D Additionally, CD36 is upregulated in tumor-infiltrating Tregs, enhancing fatty acid uptake and fatty acid oxidation (FAO). This adaptation allows Tregs to survive and function effectively in the lactate-rich and nutrient-deprived TME. Treg: regulatory T cell; TME: tumor microenvironment; OSCC: oral squamous cell carcinoma; Trp: tryptophan; Kyn: kynurenines; AHR: aryl hydrocarbon receptor; PI3K: phosphoinositide 3-kinases; AKT: protein kinase B; mTOR: mammalian target of rapamycin; PTEN: phosphate and tensin homologue; IDO1: indoleamine 2, 3-dioxygenase 1; FAO: fatty acid oxidation