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. 2023 Jan 4;30:1. doi: 10.1186/s12929-022-00894-z

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© The Author(s) 2023

Open AccessThis 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 licence, and indicate if changes were made. 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/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Epigenetic regulation of the immune response in the tumor microenvironment. DNA methylation and histone modification regulate the tumor immune response in the TME. The epigenetic mechanisms of DNA methylation induced by DNMT, transcriptional suppression by EZH2, and HDAC play crucial roles in immune-related signal inactivation, immune cell recruitment, antigen processing and presentation, and immune cell exhaustion by suppressing the expression of ERVs, MHC I genes, antigen processing machinery, and cancer testis antigens in the TME. TME: tumor microenvironment; IFNs: interferons