Several lines of evidence point towards the central role of interleukin 23 (IL-23) as a crucial inflammatory mediator in the pathogenesis of spondyloarthritis-a group of inflammatory arthritic diseases whose symptoms span the skin, gastrointestinal tract and joints. While therapeutic blockade of IL-23 proved successful in the treatment of inflammatory bowel disease, psoriatic skin disease and peripheral spondyloarthritis it failed in patients suffering from spondyloarthritis with predominantly axial involvement. Here we review state-of-the-art discoveries on IL-23 signalling pathways across target tissues involved in spondyloarthritis. We discuss the discrepancies in resident IL-23 responding cells and their downstream activities across skin, gut and joint that shape the unique immunological landscape of spondyloarthritis.
Zuzanna Łukasik, Eric Gracey, Koen Venken, Christopher Ritchlin, Dirk Elewaut