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. 2021 Mar 30;12:652160. doi: 10.3389/fimmu.2021.652160

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Copyright © 2021 Maes, Mondino, Lasarte, Agirre, Vanderkerken, Prosper and Breckpot

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Epigenetic regulation of CD4⁺ T cell differentiation. CD4⁺ T cell memory formation: During memory formation, remodeling of H3K4 methylation (green) marks takes place together with the removal of repressive H3K27me3 (red) marks in genes of the JAK-STAT pathway. Moreover, permissive H3K4me3 (green) and H3K27Ac (purple) marks are present in genes related to CD4⁺ T cell function. CD4⁺ T cell polarization: T_H1 polarization is controlled by EZH2 that silences T_H2-related genes and vice versa. KDM6B favors T_H1 polarization by positive regulation of T_H1-related genes while KMT1E negatively regulates IFNG and Tbx21 (T-bet) gene expression. HDAC1 and 11 are general inhibitors of CD4⁺ T cell function through silencing of cytokine production, Eomes and Tbx21 (T-bet). Epigenetic regulation of FOXP3 expression in Treg: FOXP3 expression is regulated by epigenetic processes in Treg including (i) exchange of repressive HDAC5 and SIRT 1 for a permissive CPB/p300 (HAT) complex, (ii) permissive H3K4me3 (green) and H3 lysine acetylation (purple) in a TGFβ response element (CNS1), (iii) TET2 dependent DNA demethylation of a 5’UTR region (CNS2), and (iii) H3K4me1/2 poised state of CNS3 needed for Foxp3 expression. HDAC1, 11 and DNMT3A represent potential targets to improve CD4⁺ T cell anti-tumor immunity.