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Neutrophils produce interleukin-17B in rheumatoid synovial tissue

Journal article
Authors V. P. Kouri
J. Olkkonen
M. Ainola
T. F. Li
Lena Björkman
Y. T. Konttinen
J. Mandelin
Published in Rheumatology
Volume 53
Issue 1
Pages 39-47
ISSN 1462-0324
Publication year 2014
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 39-47
Language en
Links dx.doi.org/10.1093/rheumatology/ket...
Keywords cytokines, fibroblasts, inflammation, neutrophils, rheumatoid arthritis
Subject categories Rheumatology and Autoimmunity

Abstract

Objective: T helper 17 (Th17) and mast cells produce IL-17A in RA and critically contribute to the pathogenesis of RA. However, the complete IL-17 cytokine profile in RA is unknown. The aim of the study was to systematically study the expression of IL-17 family cytokines in RA. Methods: The expression of all IL-17 cytokines in RA synovium and pannus as well as in the synovium of OA was determined using quantitative RT-PCR (qRT-PCR). IL-17A and IL-17B were immunostained. Peripheral blood neutrophils were analysed for IL-17B. The effect of IL-17B alone or in combination with TNF-α was tested in vitro on fibroblasts and endothelial cells. Results: In all tissues IL-17B was the most expressed IL-17 family cytokine, found in lining but most strongly expressed in human neutrophil elastase containing polymorphonuclear cells. This pattern was distinct from that of IL-17A, which was found in mast cell tryptase immunoreactive cells. Circulating neutrophils contained IL-17B, verifying the in vivo results. Fibroblasts up-regulated the expression of IL-17RB, a putative receptor of IL-17B, after TNF-α stimulation. IL-17B significantly enhanced TNF-α-induced production of G-CSF and IL-6 in fibroblasts. Conclusion: IL-17B, which is present in synovium, may contribute to the pathogenesis of RA. IL-17B can enhance the effects of TNF-α on the production of cytokines and chemokines that control immune cell trafficking and neutrophil homeostasis in the inflamed tissues. © The Author 2013. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.

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