Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ.docVIP

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Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ.doc

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Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ

Available online /content/11/4/R122 Research article Open Access Vol 11 No 4 Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ Hilde Kelchtermans1, Evelien Schurgers1, Lies Geboes1, Tania Mitera1, Jo Van Damme2, Jacques Van Snick3, Catherine Uyttenhove3 and Patrick Matthys1 1Laboratories of Immunobiology, Rega Institute, Faculty of Medicine, Katholieke Universiteit Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium 2Molecular Immunology, Rega Institute, Faculty of Medicine, Katholieke Universiteit Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium 3Ludwig Institute for Cancer Research, Brussels Branch, Cellular Genetics and Experimental Units, Christian de Duve Institute of Cellular Pathology, Université Catholique de Louvain, Avenue Hippocrate 75, B-1200 Brussels, Belgium Corresponding author: Patrick Matthys, Patrick.Matthys@rega.kuleuven.be Received: 3 Mar 2009 Revisions requested: 9 Apr 2009 Revisions received: 29 Jul 2009 Accepted: 17 Aug 2009 Published: 17 Aug 2009 Arthritis Research Therapy 2009, 11:R122 (doi:10.1186/ar2787) This article is online at: /content/11/4/R122 ? 2009 Kelchtermans et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction Interleukin (IL)-17 is a pro-inflammatory cytokine in rheumatoid arthritis (RA) and collagen-induced arthritis (CIA). Since interferon (IFN)-γ inhibits Th17 cell development, IFN-γ receptor knockout (IFN-γR KO) mice develop CIA more readily. We took advantage of this model to analyse the mechanisms of action of IL-17 in arthritis. The role of IFN-γ on the effector mechanisms of IL-17 in an in vitro system was also investigated. splenic expansion of