{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T19:26:09Z","timestamp":1791919569093,"version":"4.3.4"},"reference-count":34,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,2,18]],"date-time":"2021-02-18T00:00:00Z","timestamp":1613606400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Axial spondyloarthritis is a prevalent form of chronic arthritis which is related to psoriatic arthritis and skin psoriasis. TNF and IL-17A as well as IL-17F are key cytokines contributing to the pathobiology of this disease, as evidence by the therapeutic efficacy of inhibition of these factors. Despite the evidence that IL-23 acts as an upstream driver of Th17 cells, the T lymphocytes producing IL-17, and that IL-23 inhibition shows profound efficacy in psoriasis, blocking IL-23 failed to show any evidence of clinical efficacy in axial spondyloarthritis. In this viewpoint article, we revisit the reasons-to-believe in a role of IL-23 in the pathobiology of axial spondyloarthritis, discuss what we have learned on the pathobiology of this disease in general and on the function of the IL-23\/IL-17 axis in particular, and share a handful of lessons learned that are of relevance for the translation of emerging biological insights into clinical therapeutics.<\/jats:p>","DOI":"10.3389\/fimmu.2020.623874","type":"journal-article","created":{"date-parts":[[2021,2,20]],"date-time":"2021-02-20T07:50:48Z","timestamp":1613807448000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":40,"title":["IL-23 Inhibition in Ankylosing Spondylitis: Where Did It Go Wrong?"],"prefix":"10.3389","volume":"11","author":[{"given":"Dominique","family":"Baeten","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iannis E.","family":"Adamopoulos","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,2,18]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(11)60071-8","article-title":"Spondyloarthritis","volume":"377","author":"Dougados","year":"2011","journal-title":"Lancet"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1097\/BOR.0b013e3283534df4","article-title":"Pathogenesis of spondyloarthritis: autoimmune or autoinflammatory","volume":"24","author":"Ambarus","year":"2012","journal-title":"Curr Opin Rheumatol"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90512-d","article-title":"Spontaneous inflammatory disease in transgenic rats expressing HLA-B27 and human beta 2m: an animal model of HLA-B27-associated human disorders","volume":"63","author":"Hammer","year":"1990","journal-title":"Cell"},{"key":"B4","doi-asserted-by":"publisher","first-page":"797","DOI":"10.1016\/j.berh.2018.07.012","article-title":"The role of HLA-B*27 in spondyloarthritis","volume":"31","author":"Colbert","year":"2017","journal-title":"Best Pract Res Clin Rheumatol"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1505066","article-title":"MEASURE 1 Study Group; MEASURE 2 Study. 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