Epigenetic Control of Regulatory T Cell Stability and Function: Implications for Translation

被引：29

作者：

Joudi, Anthony M. ^{[1
,2
]}

Reyes Flores, Carla P. ^{[1
,2
]}

Singer, Benjamin D. ^{[1
,2
,3
,4
]}

机构：

[1] Northwestern Univ, Feinberg Sch Med, Dept Med, Div Pulm & Crit Care Med, Chicago, IL 60611 USA

[2] Northwestern Univ, Canning Thorac Inst, Feinberg Sch Med, Chicago, IL 60611 USA

[3] Northwestern Univ, Dept Biochem & Mol Genet, Feinberg Sch Med, Chicago, IL 60611 USA

[4] Northwestern Univ, Simpson Querrey Inst Epigenet, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

FRONTIERS IN IMMUNOLOGY | 2022年 / 13卷

关键词：

regulatory T cells; plasticity; inflammation; epigenetics; DNA methylation; therapeutics; TRANSCRIPTION FACTOR FOXP3; MEDIATOR COMPLEX; EXPRESSION; LINEAGE; DEMETHYLATION; GENERATION; PROMOTES; INHIBITION; PLASTICITY; EXPANSION;

D O I：

10.3389/fimmu.2022.861607

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

FoxP3(+) regulatory T (Treg) cells maintain immune homeostasis, promote self-tolerance, and have an emerging role in resolving acute inflammation, providing tissue protection, and repairing tissue damage. Some data suggest that FoxP3(+) T cells are plastic, exhibiting susceptibility to losing their function in inflammatory cytokine-rich microenvironments and paradoxically contributing to inflammatory pathology. As a result, plasticity may represent a barrier to Treg cell immunotherapy. Here, we discuss controversies surrounding Treg cell plasticity and explore determinants of Treg cell stability in inflammatory microenvironments, focusing on epigenetic mechanisms that clinical protocols could leverage to enhance efficacy and limit toxicity of Treg cell-based therapeutics.

引用

页数：11

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