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. 2024 Jan 30;16:9. doi: 10.1038/s41368-023-00267-8

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© The Author(s) 2024

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. 11 — Cancer cell-inflammatory cancer-associated fibroblasts (iCAFs)-regulatory T cells (Treg) recruitment in hypermetabolic oral squamous cell carcinoma (OSCC). a This correlation scatter plot shows a strong positive correlation between SLC16A1 and HIF1A, HIF1A and CXCL12, CAF infiltration and CXCL12, and CXCL12 and Treg infiltration in OSCC samples. b The TIDE algorithm predicted that immune checkpoint blockade-responsive OSCC tumor samples had higher scores for metabolic signature, CXCL12, HIF1A, and SLC16A1 expression compared to non-responsive samples. c In hypermetabolic OSCC samples, lactate utilization (SLC16A1), iCAF, HIF1A, CXCL12, and Treg chemotaxis contribute to immune suppression in the tumor microenvironment. *P < 0.05, **P < 0.01, ***P < 0.001, ***P < 0.000 1