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Mediators of Inflammation
Volume 2017 (2017), Article ID 1567120, 10 pages
Research Article

IL-34 Upregulated Th17 Production through Increased IL-6 Expression by Rheumatoid Fibroblast-Like Synoviocytes

1Department of Immunology, College of Basic Medical Science, Dalian Medical University, Liaoning, China
2Department of Rheumatology and Immunology, The Third Affiliated Hospital of Hebei Medical University, Hebei, China
3Department of Microecology, College of Basic Medical Science, Dalian Medical University, Liaoning, China
4Department of Rheumatology and Immunology, The Second Affiliated Hospital of Dalian Medical University, Liaoning, China

Correspondence should be addressed to Fang Li and Xia Li

Received 30 September 2016; Revised 28 December 2016; Accepted 20 April 2017; Published 4 June 2017

Academic Editor: Sandra Helena Penha Oliveira

Copyright © 2017 Bing Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Rheumatoid arthritis (RA) is a chronic autoimmune disease which is characterized by synovial inflammation and cartilage damage for which causes articular dysfunction. Activation of fibroblast-like synoviocytes (FLS) is a critical step that promotes disease progression. In this study, we aimed to explore the effect of interleukin-34 (IL-34) on RA FLS as a proinflammatory factor and IL-34-stimulated FLS on the production of Th17. We found that serum IL-34 levels were increased compared to those of the healthy controls and had positive correlations with C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), and anticyclic citrullinated peptide (CCP) antibody accordingly. CSF-1R was also highly expressed on RA FLS. The interaction of IL-34 and CSF-1R promoted a dramatic production of IL-6 by FLS through JNK/P38/NF-κB signaling pathway. Further, the IL-34-stimulated IL-6 secretion by RA FLS was found to upregulate the number of Th17. The treatment of IL-6R antagonist could attenuate the production of Th17 mediated by IL-34-stimulated RA FLS. Our results suggest that the increased IL-34 levels were closely related to the disease activity of RA. Additionally, the overexpression of IL-6 in the IL-34-stimulated FLS promoted the generation of Th17. Therefore, IL-34 was supposed to be involved in the pathogenesis of RA. The inhibition of IL-34 might provide a novel target for therapies of RA.