Role of Interleukin-36 in inflammatory joint diseases.
10.3724/zdxbyxb-2023-0034
- Author:
Cunyi WANG
1
;
Ji'an HU
2
;
Jiejun SHI
3
Author Information
1. Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou 310006, China. zjuwcy@foxmail.com.
2. Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou 310006, China. hja@zju.edu.cn.
3. Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou 310006, China. sjiejun2013@163.com.
- Publication Type:Journal Article
- Keywords:
Interleukin-36;
Osteoarthritis;
Psoriatic arthritis;
Review;
Rheumatoid arthritis
- MeSH:
Humans;
Interleukins;
Arthritis, Rheumatoid;
Osteoarthritis/pathology*;
Arthritis, Psoriatic/metabolism*;
Cytokines
- From:
Journal of Zhejiang University. Medical sciences
2023;52(2):249-259
- CountryChina
- Language:English
-
Abstract:
Interleukin (IL)-36 is a family of cytokines that belongs to the larger IL-1 superfamily. IL-36 agonist/antagonist binds to the interleukin-36 receptor involving in physiological inflammation regulation and pathogenesis of many inflammatory diseases. In inflammatory joint diseases, the expression of IL-36 changes, and some studies have initially explored the role of IL-36 in these diseases. In psoriatic arthritis, IL-36 signal mediates plasma cell and fibroblast-like synoviocyte crosstalk presenting IL-36 agonist/antagonist imbalance. In rheumatoid arthritis, IL-36 agonists induce fibroblast-like synoviocyte to produce pro-inflammatory factors, while IL-36 antagonist deficiency leads to lesion progression. In osteoarthritis, IL-36 agonists induce chondrocytes to produce catabolic enzymes and pro-inflammatory factors. This article reviews the expression and function of IL-36 in different inflammatory joint diseases to provide a reference for revealing their pathogenic mechanisms and discovering therapeutic targets.
