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白细胞介素-35在类风湿关节炎中的发病机制及作用

Pathogenesis and Function of Interleukin-35 in Rheumatoid Arthritis.

作者信息

Xin Pan Lin, Jie Li Fan, Cheng Qian, Bin Du Yi, Dan Cheng Wen

机构信息

School of Life Sciences, Anhui Medical University, Hefei, China.

Department of Orthopedic, Third Affiliated Hospital of Anhui Medical University, Hefei, China.

出版信息

Front Pharmacol. 2021 May 13;12:655114. doi: 10.3389/fphar.2021.655114. eCollection 2021.

DOI:10.3389/fphar.2021.655114
PMID:34054534
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8155723/
Abstract

It is well known that RA (Rheumatoid arthritis) is an autoimmune disease characterized by multiple and symmetric arthropathy. The main pathological features of RA are synovial hyperplasia, angiogenesis, pannus formation, inflammatory cell infiltration, articular cartilage, bone destruction, and ultimately joint dysfunction, even deformity. IL-35 (Interleukin-35) is a new member of the IL-12 (Interleukin-12) family, which is an immunosuppressive and anti-inflammatory cytokine secreted mainly by Treg (T regulatory cells). There is evidence suggested that IL-35 can attenuate the progression of RA through influencing the immune and pathological process. It suggests that IL-35 played an important role in the pathogenesis of RA, and can be used as a potential target for the future treatment of RA. This review summarizes the recent advances of IL-35 in the pathological roles and the therapeutic potential roles in RA.

摘要

众所周知,类风湿性关节炎(RA)是一种以多发性和对称性关节病为特征的自身免疫性疾病。RA的主要病理特征是滑膜增生、血管生成、血管翳形成、炎症细胞浸润、关节软骨和骨质破坏,最终导致关节功能障碍甚至畸形。白细胞介素-35(IL-35)是白细胞介素-12(IL-12)家族的新成员,是一种主要由调节性T细胞(Treg)分泌的免疫抑制和抗炎细胞因子。有证据表明,IL-35可通过影响免疫和病理过程来减轻RA的进展。这表明IL-35在RA的发病机制中起重要作用,并可作为未来RA治疗的潜在靶点。本文综述了IL-35在RA病理作用和治疗潜在作用方面的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/647b939e5623/fphar-12-655114-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/d465913fddb7/fphar-12-655114-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/7e6490043887/fphar-12-655114-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/e6dac371cc2b/fphar-12-655114-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/647b939e5623/fphar-12-655114-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/d465913fddb7/fphar-12-655114-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/7e6490043887/fphar-12-655114-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/e6dac371cc2b/fphar-12-655114-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/8155723/647b939e5623/fphar-12-655114-g004.jpg

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Front Immunol. 2021 Feb 17;12:607315. doi: 10.3389/fimmu.2021.607315. eCollection 2021.
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Clin Transl Med. 2021 Feb;11(2):e309. doi: 10.1002/ctm2.309.
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Association of IL-35 expression and gene polymorphisms in rheumatoid arthritis.
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Heliyon. 2024 Aug 30;10(17):e37257. doi: 10.1016/j.heliyon.2024.e37257. eCollection 2024 Sep 15.
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Br J Cancer. 2024 Jun;130(12):2016-2026. doi: 10.1038/s41416-024-02702-x. Epub 2024 May 4.
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