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Updated: Jun 12, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
The role of interleukin-17 in mediating joint destruction in rheumatoid arthritis
Xia Li1, Feng-lai Yuan, Wei-guo Lu
1The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu 214041, China.
Abstract:
Rheumatoid arthritis (RA) is a chronic, persistent inflammatory joint disease with systemic involvement that affects about 1% of the world's population, that ultimately leads to the progressive destruction of joint. Effective medical treatment for joint destruction in RA is lacking because the knowledge about molecular mechanisms leading to joint destruction are incompletely understood. It has been confirmed that cytokine-mediated immunity plays a crucial role in the pathogenesis of various autoimmune diseases including RA. Recently, IL-17 was identified, which production by Th17 cells. IL-17 has proinflammatory properties and may promote bone and joint damage through induction of matrix metalloproteinases and osteoclasts. In mice, intra-articular injection of IL-17 into the knee joint results in joint inflammation and damage. In addition, it has been shown that blocking IL-17/IL-17R signaling is effective in the control of rheumatoid arthritis symptoms and in the prevention of joint destruction. In this article, we will briefly discuss the biological features of IL-17/IL-17R and summarize recent advances on the role of IL-17/IL-17R in the pathogenesis and treatment of joint destruction in RA.
Insights
Interleukin-17 (IL-17) signaling contributes to rheumatoid arthritis (RA) joint destruction. Blocking IL-17/IL-17R effectively controls RA symptoms and prevents joint damage.
Area of Science:
- Immunology
- Rheumatology
- Molecular Biology
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease affecting 1% of the global population, leading to progressive joint destruction.
- Current treatments for joint destruction in RA are limited due to incomplete understanding of its molecular mechanisms.
- Cytokine-mediated immunity, particularly involving Interleukin-17 (IL-17), is implicated in the pathogenesis of autoimmune diseases like RA.
Purpose of the Study:
- To discuss the biological characteristics of the IL-17/IL-17R pathway.
- To summarize recent findings on the role of IL-17/IL-17R in the pathogenesis of joint destruction in RA.
- To review the therapeutic potential of targeting IL-17/IL-17R for RA treatment.
Main Methods:
- Review of existing literature on IL-17 biology and its role in autoimmune diseases.
- Analysis of studies investigating IL-17's effects on joint inflammation and bone/joint damage.
- Examination of research on the efficacy of IL-17/IL-17R signaling blockade in preclinical models of RA.
Main Results:
- IL-17, produced by Th17 cells, exhibits pro-inflammatory properties that can exacerbate bone and joint damage.
- IL-17 promotes joint destruction via the induction of matrix metalloproteinases and osteoclasts.
- Experimental models show intra-articular IL-17 injection causes knee joint inflammation and damage in mice.
- Blocking the IL-17/IL-17R pathway has demonstrated effectiveness in managing RA symptoms and preventing joint destruction.
Conclusions:
- The IL-17/IL-17R pathway plays a significant role in the pathogenesis of joint destruction in rheumatoid arthritis.
- Targeting IL-17/IL-17R signaling represents a promising therapeutic strategy for controlling RA progression and preventing joint damage.
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