gms | German Medical Science

43. Kongress der Deutschen Gesellschaft für Rheumatologie, 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie, 25. Wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie

02.-05. September 2015, Bremen

IL-17A does not contribute to the impact of the sympathectic nervous system on experimental arthritis

Meeting Abstract

  • Matthias Ebbinghaus - Universitätsklinikum Jena, Institut für Physiologie I, Jena
  • Susanne Hensellek - Universitätsklinikum Jena, Institut für Physiologie I, Jena
  • Firas Subhi Salah - Universitätsklinikium Jena, Institut für Physiologie I, Jena
  • Rolf Bräuer - Universitätsklinikum Jena, Institut für Pathologie, Jena
  • Hans-Georg Schaible - Universitätsklinikum Jena, Institut für Physiologie I, Jena

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 43. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh); 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh); 25. wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Bremen, 02.-05.09.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocER.26

doi: 10.3205/15dgrh080, urn:nbn:de:0183-15dgrh0802

Veröffentlicht: 1. September 2015

© 2015 Ebbinghaus et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe



Introduction: Interleukin 17 (IL-17), a current target for the therapy of several inflammatory diseases, is also assumed to be a mediator of inflammation in experimental models of arthritis. In murine antigen-induced arthritis (AIA) a strong anti-inflammatory effect was achieved by systemic sympathectomy in C57BL/6J mice. This effect was accompanied by a significant reduction of Th17 responses. In addition, lymphocytes produce less IL-17 after antagonistic beta-adrenergic treatment in vitro. This raised the question whether IL-17 is causally involved in the proinflammatory role of the sympathetic nervous system in AIA.

Methods: Monoarticular antigen-induced arthritis (AIA) was induced in preimmunized C57BL/6J mice and in IL-17-/- mice [1]. Chemical sympathectomy with 6-hydroxydopamine was carried out before AIA elicitation (day -1). In the course of AIA the severity of inflammation (joint swelling, histopathology) was monitored and the release of cytokines and calcitonin gene-related peptide (CGRP) in different tissues was determined by ELISA. In acute AIA the number of splenic T helper cells was determined by FACS analysis. Additionally IL-17-/- mice were checked for the expression of IL-17 subtypes by PCR.

Results: First we found that IL-17-/- mice express all subtypes of IL-17 (B, C, D, E, F) except subtype “A”. In AIA IL-17-/- mice showed severe signs of inflammation similar as wild type mice, and sympathectomy in the absence of IL-17A still acted anti-inflammatory. Furthermore, in IL-17-/- mice, significantly less IL-2, IL-6 and IFNγ was measured at the inflamed joint after sympathectomy and the number of splenic T helper 1 and T regulatory cells in IL-17-/- mice was decreased after sympathectomy. But in contrast to wild-type mice, lymphocytes derived from arthritic IL-17-/- mice did not produce less proinflammatory cytokines following previous sympathectomy.

Conclusion: Taken together we found no evidence that IL-17A is essential for sympathetic neuro-immune interactions influencing the severity of AIA. Further studies have to clarify the role of both sympathectomy and IL-17A in the local effects in the joint and in the general immune response.


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