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Abstract Number: 1156

Th17 Cytokines Regulate Osteoclastogenesis in Rheumatoid Arthritis

MIN-YOUNG JUNG1, Hae-Rim Kim2, HYUN-SOOK KIM3, HO-YOUN KIM1 and Sang Heon Lee4, 1Konkuk university hospital, Seoul, South Korea, 2Division of Rheumatology, Konkuk University School of Medicine, Seoul, South Korea, 3Soonchenhyang university school of medicine, Seoul, South Korea, 4Konkuk University Hospital, Seoul, South Korea

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: cytokines, interleukins (IL), osteoclastogenesis, osteoclasts and rheumatoid arthritis (RA)

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Session Information

Date: Monday, November 9, 2015

Session Title: Cytokines, Mediators, Cell-cell Adhesion, Cell Trafficking and Angiogenesis Poster II

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: This study aimed to determine the regulatory effect of Th17 cytokines on osteoclastogenesis in rheumatoid arthritis (RA).

Methods: The expression of interleukin (IL)-17 and receptor activator of nuclear factor kappa-B ligand (RANKL) was determined in synovial tissue, fibroblast-like synoviocytes (FLS), and synovial fluids of RA patients using immunohistochemical staining, ELISA and real-time PCR. Th17 cytokines-induced RANKL expression was studied in RA FLS by using real-time PCR, luciferase activity assays, and western blot. Human peripheral blood monocytes were cultured with macrophage colony-stimulating factor (M-CSF) and Th17 cytokines, following which osteoclastogenesis was evaluated by counting the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells. Osteoclastogenesis was also evaluated after human monocytes were co-cultured with IL-17-prestimulated FLS.

Results: There was significant correlation between RANKL and IL-17 levels in RA synovial fluid. IL-17, IL-21, and IL-22 increased the expression of RANKL mRNA in RA FLS and the IL-17-induced RANKL expression decreased by the inhibition of Act1, TRAF6, NF-κB and AP-1. Th17 cytokines and IL-17-prestimulated FLS induced osteoclastogenesis from monocytes in the absence of exogenous RANKL. The osteoclastic effect was reduced by inhibition of TNF-a.

Conclusion: Th17 cytokines have a dual effect on osteoclastogenesis in RA: direct induction of osteoclastogenesis from monocytes and upregulation of RANKL production in RA FLS. This Th17 cytokine/RANKL axis could be a potential therapeutic target for bone destruction in RA.


Disclosure: M. Y. JUNG, None; H. R. Kim, None; H. S. KIM, None; H. Y. KIM, None; S. H. Lee, None.

To cite this abstract in AMA style:

JUNG MY, Kim HR, KIM HS, KIM HY, Lee SH. Th17 Cytokines Regulate Osteoclastogenesis in Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/th17-cytokines-regulate-osteoclastogenesis-in-rheumatoid-arthritis/. Accessed January 17, 2021.
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