表观修饰在特应性皮炎发病中的作用

doi:10.35541/cjd.20220088

中华皮肤科杂志 ›› 2023, Vol. 56 ›› Issue (12): 1167-1169.doi: 10.35541/cjd.20220088

表观修饰在特应性皮炎发病中的作用

宋旷楠^1，2 张思平²

¹皖南医学院，芜湖 241002；²中国科学技术大学附属第一医院（安徽省立医院）皮肤科，合肥 230001

收稿日期:2022-02-10 修回日期:2022-09-04 发布日期:2023-12-05
通讯作者: 张思平 E-mail:zh_siping@126.com
基金资助:
安徽省自然科学基金（1808085MH259）

Role of epigenetics in the pathogenesis of atopic dermatitis

Song Kuangnan^1,2, Zhang Siping²

¹Wannan Medical College, Wuhu 241002, Anhui, China; ²Department of Dermatology, the First Affiliated Hospital of USTC（Anhui Provincial Hospital）, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China

Received:2022-02-10 Revised:2022-09-04 Published:2023-12-05
Contact: Zhang Siping E-mail:zh_siping@126.com
Supported by:
Anhui Provincial Natural Science Foundation（1808085MH259）

摘要/Abstract

摘要： 【摘要】基因表观修饰在不改变DNA序列的情况下，能够开启或关闭基因信息表达的程序，其机制主要包括DNA甲基化、组蛋白修饰和miRNA调控。一系列研究显示，表观遗传调控参与特应性皮炎的发病。本文简要综述基因表观修饰在特应性皮炎发病机制中的作用。

关键词: 皮炎, 特应性, 表观修饰, 皮肤屏障, 免疫细胞

Abstract: 【Abstract】 Gene epigenetic modification can turn on and off the program of gene expression without changing the DNA sequence, and the underlying mechanisms mainly include DNA methylation, histone modification and miRNA regulation. A series of studies have shown that epigenetic regulation is involved in the pathogenesis of atopic dermatitis. This review briefly summarizes the role of gene epigenetic modification in the pathogenesis of atopic dermatitis.

Key words: Dermatitis, atopic, Epigenetic modification, Skin barrier, Immune cells

宋旷楠张思平. 表观修饰在特应性皮炎发病中的作用[J]. 中华皮肤科杂志, 2023,56(12):1167-1169. doi:10.35541/cjd.20220088

Song Kuangnan, Zhang Siping. Role of epigenetics in the pathogenesis of atopic dermatitis[J]. Chinese Journal of Dermatology, 2023, 56(12): 1167-1169.doi:10.35541/cjd.20220088

参考文献 18

［1］	Ständer S. Atopic dermatitis［J］. N Engl J Med, 2021,384（12）:1136⁃1143. doi: 10.1056/NEJMra2023911.
［2］	Olisova OY, Kochergin NG, Kayumova LN, et al. Skin DNA methylation profile in atopic dermatitis patients: a case⁃control study［J］. Exp Dermatol, 2020,29（2）:184⁃189. doi: 10.1111/exd. 14064.
［3］	Lee J, Jang A, Seo SJ, et al. Epigenetic regulation of filaggrin gene expression in human epidermal keratinocytes［J］. Ann Dermatol, 2020,32（2）:122⁃129. doi: 10.5021/ad.2020.32.2.122.
［4］	Stevens ML, Zhang Z, Johansson E, et al. Disease⁃associated KIF3A variants alter gene methylation and expression impacting skin barrier and atopic dermatitis risk［J］. Nat Commun, 2020,11（1）:4092. doi: 10.1038/s41467⁃020⁃17895⁃x.
［5］	Liew WC, Sundaram GM, Quah S, et al. Belinostat resolves skin barrier defects in atopic dermatitis by targeting the dysregulated miR⁃335:SOX6 axis［J］. J Allergy Clin Immunol, 2020,146（3）:606⁃620.e12. doi: 10.1016/j.jaci.2020.02.007.
［6］	Rebane A, Runnel T, Aab A, et al. MicroRNA⁃146a alleviates chronic skin inflammation in atopic dermatitis through suppression of innate immune responses in keratinocytes［J］. J Allergy Clin Immunol, 2014,134（4）:836⁃847.e11. doi: 10.1016/j.jaci.2014.05.022.
［7］	Vaher H, Runnel T, Urgard E, et al. miR⁃10a⁃5p is increased in atopic dermatitis and has capacity to inhibit keratinocyte proliferation［J］. Allergy, 2019,74（11）:2146⁃2156. doi: 10.1111/all.13849.
［8］	Meng L, Li M, Gao Z, et al. Possible role of hsa⁃miR⁃194⁃5p, via regulation of HS3ST2, in the pathogenesis of atopic dermatitis in children［J］. Eur J Dermatol, 2019,29（6）:603⁃613. doi: 10.1684/ejd.2019.3676.
［9］	Liang Y, Yu B, Chen J, et al. Thymic stromal lymphopoietin epigenetically upregulates Fc receptor γ subunit⁃related receptors on antigen⁃presenting cells and induces TH2/TH17 polarization through dectin⁃2［J］. J Allergy Clin Immunol, 2019,144（4）:1025⁃1035.e7. doi: 10.1016/j.jaci.2019.06.011.
［10］	Massimini M, Dalle Vedove E, Bachetti B, et al. Polyphenols and cannabidiol modulate transcriptional regulation of Th1/Th2 inflammatory genes related to canine atopic dermatitis［J］. Front Vet Sci, 2021,8:606197. doi: 10.3389/fvets.2021.606197.
［11］	Acevedo N, Benfeitas R, Katayama S, et al. Epigenetic alterations in skin homing CD4+CLA+ T cells of atopic dermatitis patients［J］. Sci Rep, 2020,10（1）:18020. doi: 10.1038/s41598⁃020⁃74798⁃z.
［12］	Yoshida Y, Hayakawa K, Fujishiro M, et al. Social defeat stress exacerbates atopic dermatitis through downregulation of DNA methyltransferase 1 and upregulation of C⁃C motif chemokine receptor 7 in skin dendritic cells［J］. Biochem Biophys Res Commun, 2020,529（4）:1073⁃1079. doi: 10.1016/j.bbrc.2020.06. 157.
［13］	Kumar D, Puan KJ, Andiappan AK, et al. A functional SNP associated with atopic dermatitis controls cell type⁃specific methylation of the VSTM1 gene locus［J］. Genome Med, 2017,9（1）:18. doi: 10.1186/s13073⁃017⁃0404⁃6.
［14］	Sonkoly E, Janson P, Majuri ML, et al. MiR⁃155 is overexpressed in patients with atopic dermatitis and modulates T⁃cell proliferative responses by targeting cytotoxic T lymphocyte⁃associated antigen 4［J］. J Allergy Clin Immunol, 2010,126（3）:581⁃589.e1⁃20. doi: 10.1016/j.jaci.2010.05.045.
［15］	Toyoshima S, Sakamoto⁃Sasaki T, Kurosawa Y, et al. miR103a⁃3p in extracellular vesicles from FcεRI⁃aggregated human mast cells enhances IL⁃5 production by group 2 innate lymphoid cells［J］. J Allergy Clin Immunol, 2021,147（5）:1878⁃1891. doi: 10. 1016/j.jaci.2021.01.002.
［16］	Sawada Y, Nakatsuji T, Dokoshi T, et al. Cutaneous innate immune tolerance is mediated by epigenetic control of MAP2K3 by HDAC8/9［J］. Sci Immunol, 2021,6（59）:eabe1935. doi: 10. 1126/sciimmunol.abe1935.
［17］	Ujfaludi Z, Tuzesi A, Majoros H, et al. Coordinated activation of a cluster of MMP genes in response to UVB radiation［J］. Sci Rep, 2018,8（1）:2660. doi: 10.1038/s41598⁃018⁃20999⁃6.
［18］	Kwon Y, Choi Y, Kim M, et al. HDAC6 and CXCL13 mediate atopic dermatitis by regulating cellular interactions and expression levels of miR⁃9 and SIRT1［J］. Front Pharmacol, 2021,12:691279. doi: 10.3389/fphar.2021.691279.

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表观修饰在特应性皮炎发病中的作用

Role of epigenetics in the pathogenesis of atopic dermatitis

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