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银屑病关节炎中的免疫反应和细胞因子通路:一项系统评价。

Immune response and cytokine pathways in psoriatic arthritis: A systematic review.

作者信息

Dilek Gamze, Kalcik Unan Mehtap, Nas Kemal

机构信息

Abant İzzet Baysal University Training and Research Hospital, Rheumatology Clinic, Bolu, Türkiye.

Department of Physical Medicine and Rehabilitation, Division of Rheumatology and Immunology, Sakarya University School of Medicine, Sakarya, Türkiye.

出版信息

Arch Rheumatol. 2025 Mar 17;40(1):144-156. doi: 10.46497/ArchRheumatol.2025.10934. eCollection 2025 Mar.

Abstract

OBJECTIVES

This review aims to focus on the role of innate and adaptive immune system cells and their molecular signaling pathways in the pathophysiology of clinical phenotypes of psoriatic arthritis (PsA).

MATERIALS AND METHODS

A systematic literature search was conducted in the PubMed database using the key words "psoriasis," "psoriatic arthritis," "pathogenesis," "adaptive immune system," "pathophysiology," "bone and cartilage damage," and "cytokine pathways."

RESULTS

Clinical studies and studies on adaptive and innate immune system cells and mediators that cause activation of these cells in the pathogenesis of PsA were examined. The role of cytokine pathways affecting the pathogenesis of PsA on the most common clinical phenotypes of the disease were explained in detail.

CONCLUSION

In this article, we reviewed the cytokine pathways that may contribute to the immunological pathogenesis of psoriatic arthritis. We believe that this review will contribute to a better understanding of the pathogenesis of the clinical phenotypes of the disease and to disease management.

摘要

目的

本综述旨在聚焦先天性和适应性免疫系统细胞及其分子信号通路在银屑病关节炎(PsA)临床表型病理生理学中的作用。

材料与方法

在PubMed数据库中使用关键词“银屑病”“银屑病关节炎”“发病机制”“适应性免疫系统”“病理生理学”“骨与软骨损伤”和“细胞因子通路”进行系统的文献检索。

结果

对临床研究以及关于在PsA发病机制中导致这些细胞激活的适应性和先天性免疫系统细胞及介质的研究进行了考察。详细解释了影响PsA发病机制的细胞因子通路在该疾病最常见临床表型上的作用。

结论

在本文中,我们综述了可能促成银屑病关节炎免疫发病机制的细胞因子通路。我们相信本综述将有助于更好地理解该疾病临床表型的发病机制并有助于疾病管理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06f4/12010266/fa183fd877cc/AR-2025-40-1-144-156-F1.jpg

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