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滑液作为类风湿关节炎关节微环境的关键组成部分。

Synovial Fluid as a Crucial Component of the Joint Microenvironment in Rheumatoid Arthritis.

作者信息

Ziyadullaev Shukhrat Khudaiberdievich, Khudaiberdiev Shavkat Shukhratovich, Aripova Tamara Uktamovna, Chirumbolo Salvatore, Kamalov Zaynitdin Saifitdinovich, Bjørklund Geir, Rizaev Jasur Alimdjanovich, Tashkenbaeva Eleonora Negmatovna, Khamidov Obid Abdurakhmanovich, Gaffarov Usmon Bobonazarovich

机构信息

Institute of Immunology and Human Genomics, Academy of Sciences, Tashkent 100060, Uzbekistan.

Department of Medical Lab, Medical School, Central Asian University, Tashkent 111221, Uzbekistan.

出版信息

Immune Netw. 2025 Feb 5;25(2):e2. doi: 10.4110/in.2025.25.e2. eCollection 2025 Apr.

DOI:10.4110/in.2025.25.e2
PMID:40342839
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12056296/
Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease closely associated with synovial tissue proliferation, pannus formation in small joints such as the hands, wrists, and feet, cartilage destruction, and systemic complications such as pulmonary, cardiovascular, neurological, and skeletal muscle lesions, glucocorticoid-induced osteoporosis and infections. The importance of confirming the diagnosis and determining local activity is given to the study of synovial fluid. A deep understanding of the pathological process in the joint in RA, characterized by changes in autoreactive CD4+ T cells, B cells, macrophages, inflammatory cytokines, chemokines, and autoantibodies, has now been achieved, although much remains to be explored. This article provides an updated overview of the pathogenesis of RA, revealing even more therapeutic targets for the intra-articular pathological process.

摘要

类风湿关节炎(RA)是一种全身性自身免疫性疾病,与滑膜组织增生、手部、腕部和足部等小关节的血管翳形成、软骨破坏以及肺部、心血管、神经和骨骼肌病变、糖皮质激素诱导的骨质疏松症和感染等全身性并发症密切相关。滑膜液研究对于确诊和确定局部活动情况具有重要意义。尽管仍有许多有待探索之处,但目前已经对类风湿关节炎关节中的病理过程有了深入了解,其特征为自身反应性CD4 + T细胞、B细胞、巨噬细胞、炎性细胞因子、趋化因子和自身抗体的变化。本文提供了类风湿关节炎发病机制的最新综述,揭示了更多针对关节内病理过程的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf0/12056296/6124cde45a4c/in-25-e2-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf0/12056296/be8cc313204e/in-25-e2-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf0/12056296/6124cde45a4c/in-25-e2-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf0/12056296/be8cc313204e/in-25-e2-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf0/12056296/6124cde45a4c/in-25-e2-g002.jpg

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本文引用的文献

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The Search for the Pathogenic T Cells in the Joint of Rheumatoid Arthritis: Which T-Cell Subset Drives Autoimmune Inflammation?寻找类风湿关节炎关节中的致病 T 细胞:哪个 T 细胞亚群驱动自身免疫炎症?
Int J Mol Sci. 2023 Apr 8;24(8):6930. doi: 10.3390/ijms24086930.
2
The regulation of self-tolerance and the role of inflammasome molecules.自身耐受的调节和炎症小体分子的作用。
Front Immunol. 2023 Apr 4;14:1154552. doi: 10.3389/fimmu.2023.1154552. eCollection 2023.
3
Rheumatoid arthritis chondrocytes produce increased levels of pro-inflammatory proteins.
自身免疫性疾病中的泛素样蛋白:当前证据与治疗机遇
Immune Netw. 2025 May 1;25(3):e21. doi: 10.4110/in.2025.25.e21. eCollection 2025 Jun.
类风湿性关节炎软骨细胞产生的促炎蛋白水平升高。
Osteoarthr Cartil Open. 2022 Jan 21;4(1):100235. doi: 10.1016/j.ocarto.2022.100235. eCollection 2022 Mar.
4
Rheumatoid arthritis and mitochondrial homeostasis: The crossroads of metabolism and immunity.类风湿关节炎与线粒体稳态:代谢与免疫的交叉点
Front Med (Lausanne). 2022 Sep 23;9:1017650. doi: 10.3389/fmed.2022.1017650. eCollection 2022.
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Mitochondrial Dysfunction in Rheumatoid Arthritis.类风湿关节炎中的线粒体功能障碍。
Biomolecules. 2022 Sep 1;12(9):1216. doi: 10.3390/biom12091216.
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IL-3 regulates the differentiation of pathogenic Th17 cells.白细胞介素-3 调控致病性 Th17 细胞的分化。
Eur J Immunol. 2022 Nov;52(11):1842-1858. doi: 10.1002/eji.202149674. Epub 2022 Sep 26.
7
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