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本文引用的文献

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PRMT5-Selective Inhibitors Suppress Inflammatory T Cell Responses and Experimental Autoimmune Encephalomyelitis.PRMT5选择性抑制剂可抑制炎症性T细胞反应及实验性自身免疫性脑脊髓炎。
J Immunol. 2017 Feb 15;198(4):1439-1451. doi: 10.4049/jimmunol.1601702. Epub 2017 Jan 13.
2
Arginine Methylation: The Coming of Age.精氨酸甲基化:崭露头角。
Mol Cell. 2017 Jan 5;65(1):8-24. doi: 10.1016/j.molcel.2016.11.003.
3
Interactions between genetic, lifestyle and environmental risk factors for multiple sclerosis.多发性硬化症的遗传、生活方式和环境风险因素之间的相互作用。
Nat Rev Neurol. 2017 Jan;13(1):25-36. doi: 10.1038/nrneurol.2016.187. Epub 2016 Dec 9.
4
Comprehensive mapping of 5-hydroxymethylcytosine epigenetic dynamics in axon regeneration.轴突再生中5-羟甲基胞嘧啶表观遗传动力学的全面图谱
Epigenetics. 2017 Feb;12(2):77-92. doi: 10.1080/15592294.2016.1264560. Epub 2016 Dec 5.
5
One-carbon metabolism and epigenetics.一碳代谢与表观遗传学。
Mol Aspects Med. 2017 Apr;54:28-36. doi: 10.1016/j.mam.2016.11.007. Epub 2016 Nov 19.
6
Whole-Genome DNA Methylation Analysis of Peripheral Blood Mononuclear Cells in Multiple Sclerosis Patients with Different Disease Courses.不同病程多发性硬化症患者外周血单个核细胞的全基因组DNA甲基化分析
Acta Naturae. 2016 Jul-Sep;8(3):103-110.
7
The neuronal metabolite NAA regulates histone H3 methylation in oligodendrocytes and myelin lipid composition.神经元代谢物NAA调节少突胶质细胞中的组蛋白H3甲基化和髓磷脂脂质组成。
Exp Brain Res. 2017 Jan;235(1):279-292. doi: 10.1007/s00221-016-4789-z. Epub 2016 Oct 5.
8
Suppressive effects of tumor cell-derived 5'-deoxy-5'-methylthioadenosine on human T cells.肿瘤细胞源性5'-脱氧-5'-甲硫基腺苷对人T细胞的抑制作用
Oncoimmunology. 2016 Jun 10;5(8):e1184802. doi: 10.1080/2162402X.2016.1184802. eCollection 2016 Aug.
9
Proteome-wide analysis of arginine monomethylation reveals widespread occurrence in human cells.全蛋白质组精氨酸单甲基化分析揭示其在人类细胞中广泛存在。
Sci Signal. 2016 Aug 30;9(443):rs9. doi: 10.1126/scisignal.aaf7329.
10
The histone demethylase inhibitor GSK-J4 limits inflammation through the induction of a tolerogenic phenotype on DCs.组蛋白去甲基化酶抑制剂 GSK-J4 通过诱导 DC 上的耐受表型来限制炎症。
J Autoimmun. 2016 Dec;75:105-117. doi: 10.1016/j.jaut.2016.07.011. Epub 2016 Aug 12.

甲基化在多发性硬化症中的新作用:超越DNA。

Emerging Role for Methylation in Multiple Sclerosis: Beyond DNA.

作者信息

Webb Lindsay M, Guerau-de-Arellano Mireia

机构信息

School of Health and Rehabilitation Sciences, Division of Medical Laboratory Science, College of Medicine, Wexner Medical Center, Ohio State University, Columbus, OH 43210, USA; Biomedical Sciences Graduate Program, Ohio State University, Columbus, OH 43210, USA.

School of Health and Rehabilitation Sciences, Division of Medical Laboratory Science, College of Medicine, Wexner Medical Center, Ohio State University, Columbus, OH 43210, USA; Department of Microbial Infection and Immunity, Ohio State University, Columbus, OH 43210, USA; Department of Neuroscience, Ohio State University, Columbus, OH 43210, USA; Institute of Behavioral Medicine Research, Ohio State University, Columbus, OH 43210, USA.

出版信息

Trends Mol Med. 2017 Jun;23(6):546-562. doi: 10.1016/j.molmed.2017.04.004. Epub 2017 May 4.

DOI:10.1016/j.molmed.2017.04.004
PMID:28478950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5492960/
Abstract

Multiple Sclerosis (MS) is a chronic inflammatory disease of the central nervous system. The inflammatory and neurodegenerative pathways driving MS are modulated by DNA, lysine, and arginine methylation, as evidenced by studies made possible by novel tools for methylation detection or loss of function. We present evidence that MS is associated with genetic variants and metabolic changes that impact on methylation. Further, we comprehensively review current understanding of how methylation can impact on central nervous system (CNS) resilience and neuroregenerative potential, as well as inflammatory versus regulatory T helper (Th) cell balance. These findings are discussed in the context of therapeutic relevance for MS, with broad implications in other neurologic and immune-mediated diseases.

摘要

多发性硬化症(MS)是一种中枢神经系统的慢性炎症性疾病。驱动MS的炎症和神经退行性通路受到DNA、赖氨酸和精氨酸甲基化的调节,新型甲基化检测工具或功能丧失研究证明了这一点。我们提供的证据表明,MS与影响甲基化的基因变异和代谢变化有关。此外,我们全面回顾了目前对甲基化如何影响中枢神经系统(CNS)弹性和神经再生潜力,以及炎症与调节性T辅助(Th)细胞平衡的理解。这些发现将在MS治疗相关性的背景下进行讨论,对其他神经和免疫介导的疾病具有广泛影响。