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Effects of interleukin (IL)-17A and IL-17F in human rheumatoid arthritis synoviocytes
  1. Arnaud Hot1,
  2. Pierre Miossec1
  1. 1Department of Clinical Immunology and Rheumatology, University of Lyon, Edouard Herriot Hospital, France
  1. Correspondence to Professor Pierre Miossec, Department of Clinical Immunology and Rheumatology, Immunogenomics and Inflammation Research Unit EA 4130, Hospital Edouard Herriot, 69437 Lyon Cedex 03, France; pierre.miossec{at}univ-lyon1.fr

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease where the contribution of T cells is now supported by clinical results. Among the cytokines produced by T cells, interleukin (IL)-17A (previously known as IL-17) and IL-17F constitute the signature cytokines of the newly described Th17 T helper cell subset. While the effects of IL-17A on RA synoviocytes been well described, those of IL-17F remain less studied. The present review describes the effects of IL-17A and IL-17F on synoviocytes and their contribution to RA pathogenesis. Although IL-17F is less active than IL-17A when used alone, IL-17A and IL-17F induce in synoviocytes a rather similar expression pattern in the presence of tumour necrosis factor α. They enhance their response by stabilising mRNA of cytokines and enhancing receptor expression. They increase the migration, chemokine gene expression and invasiveness of synoviocytes. They contribute to disease chronicity by inhibiting synoviocyte apoptosis. Finally, they enhance metalloprotease secretion leading to cartilage damage. These properties support the combined inhibition of IL-17A and -F to control RA inflammation and joint destruction.

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Footnotes

  • Funding This work has been supported in part by grants from the Hospices Civils de Lyon and the Region Rhône-Alpes. AH is supported by the Société Nationale de Médecine Interne.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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