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Opposing macrophage polarization programs show extensive epigenomic and transcriptional cross-talk.相反的巨噬细胞极化程序显示出广泛的表观基因组和转录相互作用。
Nat Immunol. 2017 May;18(5):530-540. doi: 10.1038/ni.3710. Epub 2017 Mar 13.
2
IFN-γ Induces Histone 3 Lysine 27 Trimethylation in a Small Subset of Promoters to Stably Silence Gene Expression in Human Macrophages.IFN-γ在一小部分启动子中诱导组蛋白3赖氨酸27三甲基化，以稳定沉默人类巨噬细胞中的基因表达。
Cell Rep. 2016 Sep 20;16(12):3121-3129. doi: 10.1016/j.celrep.2016.08.051.
3
Broad defects in the energy metabolism of leukocytes underlie immunoparalysis in sepsis.严重脓毒症患者白细胞能量代谢存在广泛缺陷，导致免疫麻痹。
Nat Immunol. 2016 Apr;17(4):406-13. doi: 10.1038/ni.3398. Epub 2016 Mar 7.
4
Lineage-specific enhancers activate self-renewal genes in macrophages and embryonic stem cells.谱系特异性增强子在巨噬细胞和胚胎干细胞中激活自我更新基因。
Science. 2016 Feb 12;351(6274):aad5510. doi: 10.1126/science.aad5510. Epub 2016 Jan 21.
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Molecular control of activation and priming in macrophages.巨噬细胞中激活与启动的分子调控
Nat Immunol. 2016 Jan;17(1):26-33. doi: 10.1038/ni.3306.
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The role of the local environment and epigenetics in shaping macrophage identity and their effect on tissue homeostasis.局部环境和表观遗传学在塑造巨噬细胞特性及其对组织稳态的影响中的作用。
Nat Immunol. 2016 Jan;17(1):18-25. doi: 10.1038/ni.3325.
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Tissue biology perspective on macrophages.组织生物学视角下的巨噬细胞。
Nat Immunol. 2016 Jan;17(1):9-17. doi: 10.1038/ni.3320.
8
Interactive Big Data Resource to Elucidate Human Immune Pathways and Diseases.用于阐明人类免疫途径和疾病的交互式大数据资源。
Immunity. 2015 Sep 15;43(3):605-14. doi: 10.1016/j.immuni.2015.08.014. Epub 2015 Sep 8.
9
Super-enhancers: Asset management in immune cell genomes.超级增强子：免疫细胞基因组中的资产管理
Trends Immunol. 2015 Sep;36(9):519-26. doi: 10.1016/j.it.2015.07.005. Epub 2015 Aug 12.
10
Interferon-γ regulates cellular metabolism and mRNA translation to potentiate macrophage activation.干扰素-γ调节细胞代谢和mRNA翻译以增强巨噬细胞活化。
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干扰素-γ通过拆解与转录因子MAF结合的增强子来抑制人巨噬细胞中的M2基因表达。

Interferon-γ Represses M2 Gene Expression in Human Macrophages by Disassembling Enhancers Bound by the Transcription Factor MAF.

作者信息

Kang Kyuho, Park Sung Ho, Chen Janice, Qiao Yu, Giannopoulou Eugenia, Berg Karen, Hanidu Adedayo, Li Jun, Nabozny Gerald, Kang Keunsoo, Park-Min Kyung-Hyun, Ivashkiv Lionel B

机构信息

Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY 10021, USA; Arthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY 10021, USA.

Arthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY 10021, USA.

出版信息

Immunity. 2017 Aug 15;47(2):235-250.e4. doi: 10.1016/j.immuni.2017.07.017.

DOI:10.1016/j.immuni.2017.07.017
PMID:28813657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5568089/
Abstract

Mechanisms by which interferon (IFN)-γ activates genes to promote macrophage activation are well studied, but little is known about mechanisms and functions of IFN-γ-mediated gene repression. We used an integrated transcriptomic and epigenomic approach to analyze chromatin accessibility, histone modifications, transcription-factor binding, and gene expression in IFN-γ-primed human macrophages. IFN-γ suppressed basal expression of genes corresponding to an "M2"-like homeostatic and reparative phenotype. IFN-γ repressed genes by suppressing the function of enhancers enriched for binding by transcription factor MAF. Mechanistically, IFN-γ disassembled a subset of enhancers by inducing coordinate suppression of binding by MAF, lineage-determining transcription factors, and chromatin accessibility. Genes associated with MAF-binding enhancers were suppressed in macrophages isolated from rheumatoid-arthritis patients, revealing a disease-associated signature of IFN-γ-mediated repression. These results identify enhancer inactivation and disassembly as a mechanism of IFN-γ-mediated gene repression and reveal that MAF regulates the macrophage enhancer landscape and is suppressed by IFN-γ to augment macrophage activation.

摘要

干扰素（IFN）-γ激活基因以促进巨噬细胞活化的机制已得到充分研究，但关于IFN-γ介导的基因抑制的机制和功能却知之甚少。我们采用综合转录组学和表观基因组学方法，分析了IFN-γ预处理的人巨噬细胞中的染色质可及性、组蛋白修饰、转录因子结合和基因表达。IFN-γ抑制了与“M2”样稳态和修复表型相对应的基因的基础表达。IFN-γ通过抑制富含转录因子MAF结合的增强子的功能来抑制基因。从机制上讲，IFN-γ通过诱导MAF、谱系决定转录因子的结合以及染色质可及性的协同抑制，拆散了一部分增强子。在从类风湿性关节炎患者分离的巨噬细胞中，与MAF结合增强子相关的基因受到抑制，揭示了IFN-γ介导抑制的疾病相关特征。这些结果确定增强子失活和拆散是IFN-γ介导的基因抑制机制，并揭示MAF调节巨噬细胞增强子景观，且被IFN-γ抑制以增强巨噬细胞活化。