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. 2018 Jan 8;8:1889. doi: 10.3389/fimmu.2017.01889

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Copyright © 2018 Wawman, Bartlett and Oo.

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) or licensor 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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Regulatory T cells are controlled by epigenetic mechanisms and T cell receptor (TCR) and interleukin-2 (IL-2) pathway. Histone acetylation facilitates FoxP3 gene expression and deacetylation inhibits gene expression. HDACi, such as butyrate, can lead to upregulation of the Treg-cell master regulatory gene, FoxP3, and enhance its function. TCR and IL-2 combined stimulation leads to PI3 kinase activation and subsequent downstream activation of mTOR signaling via Akt. Treg cells require lipogenic metabolism via the mevalonate pathway, which subsequently leads to upregulation of Treg-cell suppressive molecules cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and ICOS in mTORC1-dependent manner. HDAC, Histone deacetylase inhibitor; PI3K, phosphatidylinositol 3-kinase; Akt, Protein Kinase B; mTOR, mammalian target of rapamycin; GPCR, G protein–coupled receptor.