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Neutrophils produce interleukin-17B in rheumatoid synovial tissue

Artikel i vetenskaplig tidskrift
Författare V. P. Kouri
J. Olkkonen
M. Ainola
T. F. Li
Lena Björkman
Y. T. Konttinen
J. Mandelin
Publicerad i Rheumatology
Volym 53
Nummer/häfte 1
Sidor 39-47
ISSN 1462-0324
Publiceringsår 2014
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Sidor 39-47
Språk en
Länkar dx.doi.org/10.1093/rheumatology/ket...
Ämnesord cytokines, fibroblasts, inflammation, neutrophils, rheumatoid arthritis
Ämneskategorier Reumatologi och inflammation

Sammanfattning

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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