IL-23 and axial disease: do they come together?

Rheumatology (Oxford). 2021 Oct 19;60(Suppl 4):iv28-iv33. doi: 10.1093/rheumatology/keab617.


IL-23 is a key cytokine in the pathogenesis of spondyloarthritides, including PsA and axial spondyloarthritis, as well as related conditions, such as psoriasis and IBD. Genetic associations, animal models and translational studies in humans demonstrate the key role played by IL-23, especially when coupled with downstream overexpression of IL-17 via stimulation of T helper 17 (Th17) and other cells by IL-23. Whereas IL-23 inhibition has shown clear-cut benefit in psoriasis and peripheral manifestations of PsA, trials of IL-23 inhibitors have failed in the treatment of ankylosing spondylitis. More recently, exploratory data from PsA patients with axial symptoms suggests that improvement may occur, but needs confirmation in dedicated axial spondyloarthritis (axSpA) trials. Hypotheses for these apparently conflicting findings about IL-23 inhibition in various forms of spondylitis are discussed.

Keywords: axial psoriatic arthritis; axial spondyloarthritis; interleukin-17; interleukin-23; psoriatic arthritis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Arthritis, Psoriatic / drug therapy
  • Axial Spondyloarthritis / drug therapy
  • Axial Spondyloarthritis / immunology*
  • Clinical Trials as Topic
  • Humans
  • Interleukin-17 / metabolism
  • Interleukin-23 / antagonists & inhibitors
  • Interleukin-23 / metabolism*
  • Ustekinumab / pharmacology
  • Ustekinumab / therapeutic use


  • Interleukin-17
  • Interleukin-23
  • Ustekinumab