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自身炎症性疾病:其背后的原因及新进展有哪些?

Autoinflammatory diseases: what is behind them and what is new?

作者信息

Maalouly Michele, Saade Serena, Kurban Mazen

机构信息

Department of Internal Medicine.

Department of Dermatology.

出版信息

Dermatol Reports. 2022 Dec 29;15(2):9625. doi: 10.4081/dr.2023.9625. eCollection 2023 Jun 7.

DOI:10.4081/dr.2023.9625
PMID:37426375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10327674/
Abstract

Autoinflammatory diseases are characterized by bouts of systemic or localized inflammation in the absence of an infection. While some autoinflammatory diseases are caused by a single gene mutation, others have been shown to be multifactorial, involving a large array of genes coupled with environmental factors. Previous studies briefly elucidated the molecular mechanisms behind the many autoinflammatory diseases, focusing on the dysregulation of interleukin (IL)-1β or IL-18, nuclear factor- κB activation, and Interferons secretion. In this review, we precisely highlight the autoinflammatory disease-specific signalosomes, and we aim to provide a scaffold of the link between the various affected pathways.

摘要

自身炎症性疾病的特征是在没有感染的情况下出现全身性或局部性炎症发作。虽然一些自身炎症性疾病是由单个基因突变引起的,但其他疾病已被证明是多因素的,涉及大量基因以及环境因素。先前的研究简要阐明了许多自身炎症性疾病背后的分子机制,重点关注白细胞介素(IL)-1β或IL-18的失调、核因子-κB激活和干扰素分泌。在本综述中,我们精确地突出了自身炎症性疾病特异性信号小体,旨在提供各种受影响途径之间联系的框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/10327674/9acc2c3920a5/dr-15-2-9625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/10327674/5063a3de4062/dr-15-2-9625-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/10327674/9acc2c3920a5/dr-15-2-9625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/10327674/5063a3de4062/dr-15-2-9625-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/10327674/9acc2c3920a5/dr-15-2-9625-g002.jpg

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本文引用的文献

1
Oxidized DNA fragments exit mitochondria via mPTP- and VDAC-dependent channels to activate NLRP3 inflammasome and interferon signaling.氧化的 DNA 片段通过 mPTP 和 VDAC 依赖性通道从线粒体中逸出,以激活 NLRP3 炎性体和干扰素信号。
Immunity. 2022 Aug 9;55(8):1370-1385.e8. doi: 10.1016/j.immuni.2022.06.007. Epub 2022 Jul 13.
2
NLRP1 Inflammasome Activation in Keratinocytes: Increasing Evidence of Important Roles in Inflammatory Skin Diseases and Immunity.角质形成细胞中NLRP1炎性小体的激活:在炎症性皮肤病和免疫中重要作用的证据不断增加
J Invest Dermatol. 2022 Sep;142(9):2313-2322. doi: 10.1016/j.jid.2022.04.004. Epub 2022 May 9.
3
Molecular biology of autoinflammatory diseases.
自身炎症性疾病的分子生物学
Inflamm Regen. 2021 Oct 11;41(1):33. doi: 10.1186/s41232-021-00181-8.
4
Enhanced Inflammasome Activity in Patients with Psoriasis Promotes Systemic Inflammation.银屑病患者的炎症小体活性增强可促进全身炎症。
J Invest Dermatol. 2021 Mar;141(3):586-595.e5. doi: 10.1016/j.jid.2020.07.012. Epub 2020 Sep 5.
5
The systemic autoinflammatory disorders for dermatologists. Part 2: disease examples.皮肤科系统性自身炎症性疾病。第 2 部分:疾病示例。
Clin Exp Dermatol. 2020 Dec;45(8):967-973. doi: 10.1111/ced.14251. Epub 2020 Sep 3.
6
Toward targeting inflammasomes: insights into their regulation and activation.针对炎症小体:对其调控和激活的深入了解。
Cell Res. 2020 Apr;30(4):315-327. doi: 10.1038/s41422-020-0295-8. Epub 2020 Mar 9.
7
VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease.VDAC 寡聚体形成线粒体孔,释放 mtDNA 片段并促进狼疮样疾病。
Science. 2019 Dec 20;366(6472):1531-1536. doi: 10.1126/science.aav4011. Epub 2019 Dec 19.
8
Nakajo-Nishimura syndrome and related proteasome-associated autoinflammatory syndromes.中条-西村综合征及相关蛋白酶体相关自身炎症性综合征。
J Inflamm Res. 2019 Sep 17;12:259-265. doi: 10.2147/JIR.S194098. eCollection 2019.
9
Scoping review of biological treatment of deficiency of interleukin-36 receptor antagonist (DITRA) in children and adolescents.儿童和青少年白细胞介素-36 受体拮抗剂缺乏症(DITRA)的生物治疗的范围综述。
Pediatr Rheumatol Online J. 2019 Jul 8;17(1):37. doi: 10.1186/s12969-019-0338-1.
10
The NLRP1 inflammasome: new mechanistic insights and unresolved mysteries.NLRP1 炎性小体:新的机制见解和未解之谜。
Curr Opin Immunol. 2019 Oct;60:37-45. doi: 10.1016/j.coi.2019.04.015. Epub 2019 May 20.