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银屑病关节炎:组织靶向性炎症?

Psoriatic arthritis: tissue-directed inflammation?

机构信息

Rheumatology Unit, Department of Medicine, University of Perugia, Perugia, Italy.

Institute of Infection Immunity and Inflammation, College of MVLS, University of Glasgow, Glasgow, G128QQ, UK.

出版信息

Clin Rheumatol. 2018 Apr;37(4):859-868. doi: 10.1007/s10067-018-4012-7. Epub 2018 Feb 23.

Abstract

The clinical picture of psoriatic arthritis (PsA) is heterogeneous, potentially involving numerous organs and tissues, such as skin and joint. From a clinical point of view, discrete tissue PsA features develop and respond to treatments apparently independently. The pathogenic events occurring in the various tissues are only partially understood. Although the vast majority of known genetic predisposing factors are shared between patients with skin psoriasis (PSO) and those affected by PsA, some tissue-specific variants have been identified. Furthermore, current data suggest that the TNF pathway and IL-23/Th17 pathways may be differentially activated in distinct tissue sites. In this review, we briefly describe current knowledge on the pathogenesis of PsA in terms of genetic predisposition, environmental factors and immunology, advancing our hypothesis to explain why a common immunologic process can express itself with significant differences in various tissues.

摘要

银屑病关节炎(PsA)的临床表现具有异质性,可能涉及众多器官和组织,如皮肤和关节。从临床角度来看,离散的组织 PsA 特征发展并对治疗有明显的独立反应。对各种组织中发生的致病事件的了解还很有限。尽管绝大多数已知的遗传易感性因素在患有银屑病(PSO)的患者和受 PsA 影响的患者之间是共有的,但已经确定了一些组织特异性变体。此外,目前的数据表明,TNF 途径和 IL-23/Th17 途径可能在不同的组织部位被不同地激活。在这篇综述中,我们简要描述了目前关于 PsA 发病机制的遗传易感性、环境因素和免疫学方面的知识,提出了一个假设来解释为什么一个共同的免疫过程可以在不同的组织中表现出显著的差异。

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