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与银屑病和系统性红斑狼疮共病机制相关的分子学考量(综述)

Molecular consideration relevant to the mechanism of the comorbidity between psoriasis and systemic lupus erythematosus (Review).

作者信息

Qu Yuying, Li Dongmei, Liu Weida, Shi Dongmei

机构信息

Department of Dermatology, College of Clinical Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.

Department of Microbiology and Immunology, Georgetown University Medical Center, Washington, DC 20057, USA.

出版信息

Exp Ther Med. 2023 Aug 29;26(4):482. doi: 10.3892/etm.2023.12181. eCollection 2023 Oct.

DOI:10.3892/etm.2023.12181
PMID:37745036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10515117/
Abstract

Systemic lupus erythematosus (SLE), a common autoimmune disease with a global incidence and newly diagnosed population estimated at 5.14 (range, 1.4-15.13) per 100,000 person-years and 0.40 million people annually, respectively, affects multiple tissues and organs; for example, skin, blood system, heart and kidneys. Accumulating data has also demonstrated that psoriasis (PS) can be a systemic inflammatory disease, which can affect organs other than the skin and occur alongside other autoimmune diseases, such as inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis and SLE. The current explanations for the possible comorbidity of PS and SLE include: i) The two diseases share susceptible gene loci; ii) they share a common IL-23/T helper 17 (Th17) axis inflammatory pathway; and iii) the immunopathogenesis of the two conditions is a consequence of the interactions between IL-17 cytokines with effector Th17 cells, T regulatory cells, as well as B cells. In addition, the therapeutic efficacy of IL-17 or TNF-α inhibitors has been demonstrated in PS, and has also become evident in SLE. However, the mechanisms have not been investigated. To the best of our knowledge, there remains a lack of substantial studies on the correlation between PS and SLE. In the present review, the literature, with regards to the epidemiology, genetic predisposition, inflammatory mechanisms and treatment of the patients with both PS and SLE, has been reviewed. Further investigations into the molecular pathogenic mechanism may provide drug targets that could benefit the patients with concomitant PS and SLE.

摘要

系统性红斑狼疮(SLE)是一种常见的自身免疫性疾病,全球发病率估计为每10万人年5.14例(范围为1.4 - 15.13例),每年新诊断人数为40万人,可累及多个组织和器官,如皮肤、血液系统、心脏和肾脏。越来越多的数据还表明,银屑病(PS)可能是一种全身性炎症性疾病,可累及皮肤以外的器官,并与其他自身免疫性疾病同时发生,如炎症性肠病、多发性硬化症、类风湿性关节炎和SLE。目前对PS和SLE可能合并存在的解释包括:i)这两种疾病共享易感基因位点;ii)它们共享共同的IL - 23/T辅助性T细胞17(Th17)轴炎症途径;iii)这两种疾病的免疫发病机制是IL - 17细胞因子与效应性Th17细胞、调节性T细胞以及B细胞之间相互作用的结果。此外,IL - 17或TNF -α抑制剂在PS中的治疗效果已得到证实,在SLE中也已显现,但相关机制尚未得到研究。据我们所知,目前关于PS和SLE之间相关性的实质性研究仍然缺乏。在本综述中,我们回顾了有关PS和SLE患者的流行病学、遗传易感性、炎症机制及治疗方面的文献。对分子致病机制的进一步研究可能会提供有利于同时患有PS和SLE患者的药物靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c52/10515117/1f6d7ed7d728/etm-26-04-12181-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c52/10515117/416642fc35fc/etm-26-04-12181-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c52/10515117/1f6d7ed7d728/etm-26-04-12181-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c52/10515117/416642fc35fc/etm-26-04-12181-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c52/10515117/1f6d7ed7d728/etm-26-04-12181-g01.jpg

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