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A20 在细胞死亡、炎症和自身免疫的十字路口。

A20 at the Crossroads of Cell Death, Inflammation, and Autoimmunity.

机构信息

VIB Center for Inflammation Research, 9052 Ghent, Belgium.

Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium.

出版信息

Cold Spring Harb Perspect Biol. 2020 Jan 2;12(1):a036418. doi: 10.1101/cshperspect.a036418.

DOI:10.1101/cshperspect.a036418
PMID:31427375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6942121/
Abstract

A20 is a potent anti-inflammatory protein, acting by inhibiting nuclear factor κB (NF-κB) signaling and inflammatory gene expression and/or by preventing cell death. Mutations in the gene have been associated with a plethora of inflammatory and autoimmune pathologies in humans and in mice. Although the anti-inflammatory role of A20 is well accepted, fundamental mechanistic questions regarding its mode of action remain unclear. Here, we review new findings that further clarify the molecular and cellular mechanisms by which A20 controls inflammatory signaling and cell death, and discuss new evidence for its involvement in inflammatory and autoimmune disease development.

摘要

A20 是一种有效的抗炎蛋白,通过抑制核因子 κB(NF-κB)信号和炎症基因表达,或通过防止细胞死亡来发挥作用。基因中的突变与人类和小鼠中大量的炎症和自身免疫性疾病有关。尽管 A20 的抗炎作用已被广泛接受,但关于其作用机制的基本机制问题仍不清楚。在这里,我们回顾了新的发现,这些发现进一步阐明了 A20 控制炎症信号和细胞死亡的分子和细胞机制,并讨论了其在炎症和自身免疫性疾病发展中的新证据。

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1
A20 at the Crossroads of Cell Death, Inflammation, and Autoimmunity.A20 在细胞死亡、炎症和自身免疫的十字路口。
Cold Spring Harb Perspect Biol. 2020 Jan 2;12(1):a036418. doi: 10.1101/cshperspect.a036418.
2
A20 and Cell Death-driven Inflammation.A20 与细胞死亡驱动的炎症
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本文引用的文献

1
A20 prevents inflammasome-dependent arthritis by inhibiting macrophage necroptosis through its ZnF7 ubiquitin-binding domain.A20 通过其 ZnF7 泛素结合结构域抑制巨噬细胞坏死性凋亡来预防炎性关节炎。
Nat Cell Biol. 2019 Jun;21(6):731-742. doi: 10.1038/s41556-019-0324-3. Epub 2019 May 13.
2
Physical and functional interaction between A20 and ATG16L1-WD40 domain in the control of intestinal homeostasis.A20 和 ATG16L1-WD40 结构域在控制肠道内稳态中的物理和功能相互作用。
Nat Commun. 2019 Apr 23;10(1):1834. doi: 10.1038/s41467-019-09667-z.
3
Elevated A20 promotes TNF-induced and RIPK1-dependent intestinal epithelial cell death.A20 水平升高可促进 TNF 诱导的和 RIPK1 依赖性肠上皮细胞死亡。
Proc Natl Acad Sci U S A. 2018 Sep 25;115(39):E9192-E9200. doi: 10.1073/pnas.1810584115. Epub 2018 Sep 12.
4
Keratinocyte Expression of A20/TNFAIP3 Controls Skin Inflammation Associated with Atopic Dermatitis and Psoriasis.角质形成细胞表达 A20/TNFAIP3 可控制特应性皮炎和银屑病相关的皮肤炎症。
J Invest Dermatol. 2019 Jan;139(1):135-145. doi: 10.1016/j.jid.2018.06.191. Epub 2018 Aug 14.
5
A Case of Adult-Onset Still's Disease Caused by a Novel Splicing Mutation in Successfully Treated With Tocilizumab.一例由新型剪接突变引起的成人斯蒂尔病经托珠单抗成功治疗的病例。
Front Immunol. 2018 Jul 4;9:1527. doi: 10.3389/fimmu.2018.01527. eCollection 2018.
6
A20 and ABIN-1 synergistically preserve intestinal epithelial cell survival.A20 和 ABIN-1 协同作用以维持肠道上皮细胞的存活。
J Exp Med. 2018 Jul 2;215(7):1839-1852. doi: 10.1084/jem.20180198. Epub 2018 Jun 21.
7
A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation.A20 严格控制小胶质细胞激活并抑制依赖于炎性小体的神经炎症。
Nat Commun. 2018 May 23;9(1):2036. doi: 10.1038/s41467-018-04376-5.
8
'A20 haploinsufficiency (HA20): clinical phenotypes and disease course of patients with a newly recognised NF-kB-mediated autoinflammatory disease'.A20单倍体不足(HA20):一种新发现的核因子κB介导的自身炎症性疾病患者的临床表型和病程
Ann Rheum Dis. 2019 May;78(5):e35. doi: 10.1136/annrheumdis-2018-213347. Epub 2018 Mar 16.
9
Dissection and function of autoimmunity-associated TNFAIP3 (A20) gene enhancers in humanized mouse models.人源化小鼠模型中自身免疫相关TNFAIP3(A20)基因增强子的剖析与功能研究
Nat Commun. 2018 Feb 13;9(1):658. doi: 10.1038/s41467-018-03081-7.
10
A20 haploinsufficiency (HA20): clinical phenotypes and disease course of patients with a newly recognised NF-kB-mediated autoinflammatory disease.A20 单倍体不足(HA20):一种新发现的 NF-κB 介导的自身炎症性疾病患者的临床表型和疾病进程。
Ann Rheum Dis. 2018 May;77(5):728-735. doi: 10.1136/annrheumdis-2017-212403. Epub 2018 Jan 9.