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类风湿关节炎的两个主要细胞成分:关节滑膜中 T 细胞与成纤维样滑膜细胞的相互作用。

Two Main Cellular Components in Rheumatoid Arthritis: Communication Between T Cells and Fibroblast-Like Synoviocytes in the Joint Synovium.

机构信息

Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-Inflammatory and Immune Medicine, Hefei, China.

Department of Gynecology, The First Affiliated Hospital of Shenzhen University, Health Science Center, Shenzhen Second People's Hospital, Shenzhen, China.

出版信息

Front Immunol. 2022 Jul 1;13:922111. doi: 10.3389/fimmu.2022.922111. eCollection 2022.

DOI:10.3389/fimmu.2022.922111
PMID:35844494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9284267/
Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease that endangers the health of approximately 1% of the global population. Current RA medications on the market mainly include non-steroidal anti-inflammatory drugs, biological agents, and disease-modifying drugs. These drugs aim to inhibit the overactivated immune response or inflammation of RA, but they cannot cure RA. A better understanding of the pathogenesis of RA will provide a new understanding to search for RA targets and for drug development. The infiltration of T cells and hyper-proliferation of fibroblast-like synoviocytes (FLS) in the synovium of patients with RA are significantly upregulated. Furthermore, the abnormal activation of these two types of cells has been confirmed to promote development of the course of A by many studies. This article systematically summarizes the interactions between T cells and FLS in RA synovial tissues, including one-way/mutual regulation and direct/indirect regulation between the two. It further aims to investigate the pathogenesis of RA from the perspective of mutual regulation between T cells and FLS and to provide new insights into RA research.

摘要

类风湿关节炎(RA)是一种慢性自身免疫性疾病,大约影响全球 1%的人口的健康。目前市场上的 RA 药物主要包括非甾体抗炎药、生物制剂和疾病修饰药物。这些药物旨在抑制 RA 的过度激活免疫反应或炎症,但不能治愈 RA。更好地了解 RA 的发病机制将为寻找 RA 靶点和药物开发提供新的认识。RA 患者滑膜中 T 细胞的浸润和成纤维样滑膜细胞(FLS)的过度增殖显著上调。此外,许多研究证实,这两种细胞的异常激活可促进疾病的发展。本文系统总结了 T 细胞和 FLS 在 RA 滑膜组织中的相互作用,包括两者之间的单向/相互调节以及直接/间接调节。它进一步旨在从 T 细胞和 FLS 相互调节的角度探讨 RA 的发病机制,并为 RA 研究提供新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3f2/9284267/1501a7fd0543/fimmu-13-922111-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3f2/9284267/f5dfdad70e74/fimmu-13-922111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3f2/9284267/0b9839ec9e1b/fimmu-13-922111-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3f2/9284267/1501a7fd0543/fimmu-13-922111-g006.jpg

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