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本文引用的文献

1
Genome-wide DNA methylation patterns in naive CD4+ T cells from patients with primary Sjögren's syndrome.原发性干燥综合征患者初始 CD4+ T 细胞中的全基因组 DNA 甲基化模式。
Arthritis Rheumatol. 2014 Mar;66(3):731-9. doi: 10.1002/art.38264.
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Stimulus-triggered fate conversion of somatic cells into pluripotency.刺激触发体细胞的多能性命运转换。
Nature. 2014 Jan 30;505(7485):641-7. doi: 10.1038/nature12968.
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Multiple knockout mouse models reveal lincRNAs are required for life and brain development.多个基因敲除小鼠模型表明长链非编码核糖核酸对于生命和大脑发育是必需的。
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Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis.自身免疫性关节炎中 Foxp3+T 细胞向 TH17 细胞的病理性转化。
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Interactome maps of mouse gene regulatory domains reveal basic principles of transcriptional regulation.小鼠基因调控区域互作组图谱揭示了转录调控的基本原理。
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A special population of regulatory T cells potentiates muscle repair.调节性 T 细胞的一个特殊群体促进肌肉修复。
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Self-antigen-driven activation induces instability of regulatory T cells during an inflammatory autoimmune response.自身抗原驱动的激活导致炎症性自身免疫反应中调节性 T 细胞的不稳定性。
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The polycomb protein Ezh2 regulates differentiation and plasticity of CD4(+) T helper type 1 and type 2 cells.多梳蛋白 Ezh2 调节 CD4(+) T 辅助细胞 1 和 2 型的分化和可塑性。
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Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells.共生微生物衍生的丁酸盐诱导结肠调节性 T 细胞的分化。
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辅助性T细胞可塑性：外在和内在信号对转录组和表观基因组的影响

Helper T cell plasticity: impact of extrinsic and intrinsic signals on transcriptomes and epigenomes.

作者信息

Bonelli Michael, Shih Han-Yu, Hirahara Kiyoshi, Singelton Kentner, Laurence Arian, Poholek Amanda, Hand Tim, Mikami Yohei, Vahedi Golnaz, Kanno Yuka, O'Shea John J

机构信息

Molecular Immunology and Inflammation Branch, National Institutes of Arthritis, and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.

出版信息

Curr Top Microbiol Immunol. 2014;381:279-326. doi: 10.1007/82_2014_371.

DOI:10.1007/82_2014_371
PMID:24831346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4200396/
Abstract

CD4(+) helper T cells are crucial for autoimmune and infectious diseases; however, the recognition of the many, diverse fates available continues unabated. Precisely what controls specification of helper T cells and preserves phenotypic commitment is currently intensively investigated. In this review, we will discuss the major factors that impact helper T cell fate choice, ranging from cytokines and the microbiome to metabolic control and epigenetic regulation. We will also discuss the technological advances along with the attendant challenges presented by "big data," which allow the understanding of these processes on comprehensive scales.

摘要

CD4(+)辅助性T细胞对自身免疫性疾病和感染性疾病至关重要；然而，对其多种不同命运的认识仍在持续深入。目前正在深入研究究竟是什么控制着辅助性T细胞的分化并维持其表型稳定性。在这篇综述中，我们将讨论影响辅助性T细胞命运选择的主要因素，从细胞因子、微生物群到代谢控制和表观遗传调控。我们还将讨论技术进步以及“大数据”带来的相关挑战，这些使得我们能够在全面的尺度上理解这些过程。