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Abstract Number: 21

IL-32 and IL-17 Interact and Aggravate Osteoclastogenesis in Rheumatoid Arthritis

Bo Young Yoon1, Young-Mee Moon2, Yang-Mi Her2, Hye Jwa Oh2, Jae-Seon Lee2, Kyoung-Woon Kim3, Seon-Yeong Lee2, Yun-Ju Woo2, Kyung-Su Park2, Sung-Hwan Park4, Ho-Youn Kim2 and Mi-La Cho2, 1Inje University Ilsan Paik Hospital, Goyang, South Korea, 2Rheumatism Research Center, Catholic Research Institute of Medical Science, Catholic University of Korea, Seoul, South Korea, 3Conversant Research Consortium in Immunologic disease, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul, South Korea, 4Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul St. Mary's Hospital, Seoul, South Korea

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: interleukins (IL), osteoclasts, rheumatoid arthritis (RA) and synovial cells, synovial fluid

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Session Information

Title: Biology and Pathology of Bone and Joint

Session Type: Abstract Submissions (ACR)

Background/Purpose: Interleukin (IL)-32 and IL-17 play critical roles in pro-inflammatory responses and are highly expressed in the synovium of patients with rheumatoid arthritis (RA). We investigated not only the related induction of IL-17 and IL-32 in fibroblast-like synoviocytes (FLSs) from RA patients and T cells from healthy donors, but also the summative ability of the two cytokines to stimulate osteoclastogenesis.    

Methods: FLSs were isolated through surgical synovectomy obtained from patients with RA or osteoarthritis (OA) and peripheral blood mononuclear cells (PBMCs) were obtained from healthy donors. Splenic CD4+ and CD4– T cells and joint specimens were obtained from autoimmune arthritis mice.Real-time polymerase chain reactions were performed to evaluate the expression of IL-32, IL-17, orphan nuclear receptor Rorgt, tartrate-resistant acid phosphatase (TRAP), cathepsin K, calcitonin receptor (CTR), matrix metalloproteinase-9 (MMP9) mRNA. IL-17 protein was measured by enzyme-linked immunosorbent assay and the T helper (Th)17-expressing T cell count was detected by fluorescence-activated cell sorting. Immunohistochemical staining and TRAP staining were performed to determine the distribution of inflammatory cytokines and the presence of osteoclastogenesis.

Results: IL-17 induced the expression of IL-32 (4.3 fold) in the FLSs from RA patients, as assessed by microarray. The IL-32 and IL-17 levels in the FLSs from the RA patients were higher than those from the OA patients, and the expressions were colocalized. IL-32 production was increased by IL-17 through the nuclear factor (NF-¥êB)– kB and PI3 kinase signal pathways. When FLSs from RA patients and CD4+ T cells were cocultured, the CD4+ T cells differentiated into IL-17-producing Th17 cells, which stimulated the production of IL-32 in the FLSs. Moreover, IL-32 induced the production of IL-17 in human CD4+ T cells and also induced high expression levels of IL-17 in splenic CD4+ T cells of CIA mice. IL-32 and IL-17 were colocalized near TRAP-positive areas in joint specimens of autoimmune arthritis mouse models. IL-17 and IL-32 synergistically induced the differentiation of osteoclasts, as demonstrated by the expression of osteoclast-related genes such as TRAP, cathepsin K, CTR, and MMP9.

Conclusion: IL-17 affected the expression of IL-32 in FLSs of RA patients and IL-32 induced the production of IL-17 in CD4+ T cells. Both IL-17 and IL-32 cytokines can reciprocally influence each other’s production in RA and autoimmune arthritis models. Separately, IL-17 and IL-32 each stimulated osteoclastogenesis without RANKL. Together, the two cytokines synergistically amplified the differentiation of osteoclasts, independent of RANKL stimulation.


Disclosure:

B. Y. Yoon,
None;

Y. M. Moon,
None;

Y. M. Her,
None;

H. J. Oh,
None;

J. S. Lee,
None;

K. W. Kim,
None;

S. Y. Lee,
None;

Y. J. Woo,
None;

K. S. Park,
None;

S. H. Park,
None;

H. Y. Kim,
None;

M. L. Cho,
None.

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