You are here

  • Home
  • Archive
  • Volume 73, Issue 11
  • IL-23 expression and activation of autophagy in synovium and PBMCs of HLA-B27 positive patients with ankylosing spondylitis. Response to: ‘Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of pat…

Article Text

Article menu
Download PDFPDF
Electronic pages
Correspondence
IL-23 expression and activation of autophagy in synovium and PBMCs of HLA-B27 positive patients with ankylosing spondylitis. Response to: ‘Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis and subclinical gut inflammation’ by Ciccia et al
  1. B Neerinckx1,2,
  2. S Carter2,
  3. R Lories1,2
  1. 1Division of Rheumatology, UZ Leuven, Leuven, Belgium
  2. 2Department of Development and Regeneration, KU Leuven, Leuven, Belgium
  1. Correspondence to Dr R Lories, Division of Rheumatology, UZ Leuven, Leuven 3000, Belgium; Rik.Lories{at}med.kuleuven.be

https://doi.org/10.1136/annrheumdis-2014-206277

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    Interleukin 23 (IL-23) may play a key role in the pathogenesis of ankylosing spondylitis (AS). Patient studies reported increased serum levels of IL-23 in AS1–3 and the presence of IL-23 positive cells in facet joints of patients with AS.4 Moreover, in vivo overexpression of IL-23 in mice appears sufficient to phenocopy the human disease with inflammation and new bone formation and IL-23 receptor positive cells are found in entheses.5 The exact mechanism of how and where IL-23 production is induced and how it further contributes to the disease processes is not yet known. Different hypotheses have been proposed, such as HLA-B27 misfolding with activation of the unfolded protein response (UPR) as molecular drivers of IL-23 production. However, strong evidence of misfolding and UPR activation in patient samples is lacking.

    Ciccia et al demonstrated that HLA-B27 misfolding specifically occurs in the gut of patients with AS and is accompanied by activation of autophagy rather than by activation of the UPR. Autophagy possibly causes the …

    View Full Text

    Footnotes

    • Competing interests None.

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

    Linked Articles