FGF2 cooperates with IL-17 to promote autoimmune inflammation.

Abstract

IL-17 is a pro-inflammatory cytokine implicated a variety of autoimmune diseases. We have recently reported that FGF2 cooperates with IL-17 to protect intestinal epithelium during dextran sodium sulfate (DSS)-induced colitis. Here, we report a pathogenic role of the FGF2-IL-17 cooperation in the pathogenesis of autoimmune arthritis. Combined treatment with FGF2 and IL-17 synergistically induced ERK activation as well as the production of cytokines and chemokines in human synovial intimal resident fibroblast-like synoviocytes (FLS). Furthermore, ectopic expression of FGF2 in mouse joints potentiated IL-17-induced inflammatory cytokine and chemokine production in the tissue. In the collagen-induced arthritis (CIA) model, while ectopic expression of FGF2 in vivo exacerbated tissue inflammation and disease symptom in the wild-type controls, the effect was largely blunted in Il17a -/- mice. Taken together, our study suggests that FGF2 cooperates with IL-17 to promote the pathogenesis of autoimmune arthritis by cooperating with IL-17 to induce inflammatory response.

• Authors: Xinrui Shao, Siyuan Chen, Daping Yang, Mengtao Cao, Yikun Yao, Zhengxi Wu, Ningli Li, Nan Shen, Xiaoxia Li, Xinyang Song, Youcun Qian
• Journal: Scientific reports (Sci Rep) Vol. 7 Issue 1 Pg. 7024 (08 01 2017) ISSN: 2045-2322 [Electronic] England
• PMID: 28765647 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Interleukin-17
• Fibroblast Growth Factor 2

Topics

• Animals
• Arthritis (physiopathology)
• Autoimmune Diseases (physiopathology)
• Cells, Cultured
• Disease Models, Animal
• Fibroblast Growth Factor 2 (metabolism)
• Humans
• Inflammation (physiopathology)
• Interleukin-17 (metabolism)
• Mice
• Synoviocytes (metabolism)