Statistics from Altmetric.com
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 …
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.