Skip Navigation


Rheumatology Advance Access originally published online on June 12, 2006
Rheumatology 2007 46(1):57-64; doi:10.1093/rheumatology/kel159
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrowOA All Versions of this Article:
46/1/57    most recent
kel159v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kim, H.-R.
Right arrow Articles by Kim, H.-Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, H.-R.
Right arrow Articles by Kim, H.-Y.
Related Collections
Right arrow Rheumatoid Arthritis
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Up-regulation of IL-23p19 expression in rheumatoid arthritis synovial fibroblasts by IL-17 through PI3-kinase-, NF-{kappa}B- and p38 MAPK-dependent signalling pathways

H.-R. Kim1, M.-L. Cho2, K.-W. Kim2, J.-Y. Juhn2, S.-Y. Hwang3, C.-H. Yoon2, S.-H. Park2, S.-H. Lee1 and H.-Y. Kim2

1Department of Internal Medicine, School of Medicine, Konkuk University, Seoul and 2Rheumatism Research Center, Catholic Institutes of Medical Science, The Catholic University of Korea, Seoul and 3Graduate School of Biology and Information Technology, Institute of Genetic Engineering, Hankyung National University, Ansung, Kyonggi-Do, Korea.

Correspondence to: Ho-Youn Kim, MD, PhD, Department of Internal Medicine, Kangnam St., Mary's Hospital, The Catholic University of Korea, Banpo-Dong 505, Seocho-Gu, Seoul, Korea. E-mail: ho{at}catholic.ac.kr


  Abstract

Objective. To investigate the expression of interleukin (IL)-23p19 in human rheumatoid arthritis (RA) synovial fibroblasts and its up-regulation by IL-17 stimulation, and to define the signal pathways involved in the regulation of IL-23p19 expression in RA synovial fibroblasts.

Methods. Synovial fluid (SF) and serum levels of IL-23p19 in RA were determined by enzyme-linked immunosorbent assays. The levels of IL-23p19 mRNA and protein were measured after the RA synovial fibroblasts were treated with recombinant human IL-17 and various inhibitors of intracellular signal pathway molecules using reverse transcription (RT) polymerase chain reaction (PCR), real-time PCR and western blotting.

Results. Levels of IL-23p19 in the sera and SF were much higher in RA patients than in osteoarthritis patients or healthy controls. The expression of IL-23p19 mRNA and protein was enhanced in RA synovial fibroblasts by IL-17 stimulation. Such effects of IL-17 were completely blocked by inhibitors of phosphatidylinositol (PI)-kinase/Akt, nuclear factor (NF)-{kappa}B and p38 mitogen-activated protein kinase (MAPK). In accordance with the expression of IL-23p19, the phosphorylation of I{kappa}B, Akt and p38 MAPK in synovial fibroblasts also increased after IL-17 stimulation.

Conclusion. IL-23p19 is over-expressed in RA synovial fibroblasts and IL-17 appears to up-regulate the expression of IL-23p19 in RA synovial fibroblasts via PI3-kinase/Akt, NF-{kappa}B- and p38-MAPK-mediated pathways. These results suggest that a disruption of interaction between IL-17 and IL-23p19 may provide a new therapeutic approach in the treatment of RA.

KEY WORDS: Rheumatoid arthritis, Synovial fibroblast, IL-23, IL-17


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Rheumatology (Oxford)Home page
V. Paunovic, H. P. Carroll, K. Vandenbroeck, and M. Gadina
Signalling, inflammation and arthritis: Crossed signals: the role of interleukin (IL)-12, -17, -23 and -27 in autoimmunity
Rheumatology, June 1, 2008; 47(6): 771 - 776.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
S. R. Kim, K. S. Lee, S. J. Park, K. H. Min, K. Y. Lee, Y. H. Choe, Y. R. Lee, J. S. Kim, S. J. Hong, and Y. C. Lee
PTEN Down-Regulates IL-17 Expression in a Murine Model of Toluene Diisocyanate-Induced Airway Disease
J. Immunol., November 15, 2007; 179(10): 6820 - 6829.
[Abstract] [Full Text] [PDF]

Home page
 Sci SignalHome page
A. Linden
A Role for the Cytoplasmic Adaptor Protein Act1 in Mediating IL-17 Signaling
Sci. Signal., August 7, 2007; 2007(398): re4 - re4.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.