{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:11:52Z","timestamp":1792131112425,"version":"4.4.0"},"reference-count":52,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,6,27]],"date-time":"2014-06-27T00:00:00Z","timestamp":1403827200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2014,7]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Spondyloarthritides (SpA) occur in 1% of the population and include ankylosing spondylitis (AS) and arthropathy of inflammatory bowel disease (IBD), with characteristic spondylitis, arthritis, enthesitis, and IBD. Genetic studies implicate interleukin\u201023 (IL\u201023) receptor signaling in the development of SpA and IBD, and IL\u201023 overexpression in mice is sufficient for enthesitis, driven by entheseal\u2010resident T cells. However, in genetically prone individuals, it is not clear where IL\u201023 is produced and how it drives the SpA syndrome, including IBD or subclinical gut inflammation of AS. Moreover, it is unclear why specific tissue involvement varies between patients with SpA. We undertook this study to determine the location of IL\u201023 production and its role in SpA pathogenesis in BALB\/c ZAP\u201070\n                      <jats:sup>W163C<\/jats:sup>\n                      \u2013mutant (SKG) mice injected intraperitoneally with \u03b2\u20101,3\u2010glucan (curdlan).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Eight weeks after curdlan injection in wild\u2010type or IL\u201017A\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      SKG or BALB\/c mice, pathology was scored in tissue sections. Mice were treated with anti\u2013IL\u201023 or anti\u2013IL\u201022. Cytokine production and endoplasmic reticulum (ER) stress were determined in affected organs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In curdlan\u2010treated SKG mice, arthritis, enthesitis, and ileitis were IL\u201023 dependent. Enthesitis was specifically dependent on IL\u201017A and IL\u201022. IL\u201023 was induced in the ileum, where it amplified ER stress, goblet cell dysfunction, and proinflammatory cytokine production. IL\u201017A was pathogenic, while IL\u201022 was protective against ileitis. IL\u201022+CD3\u2212 innate\u2010like cells were increased in lamina propria mononuclear cells of ileitis\u2010resistant BALB\/c mice, which developed ileitis after curdlan injection and anti\u2013IL\u201022.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In response to systemic \u03b2\u20101,3\u2010glucan, intestinal IL\u201023 provokes local mucosal dysregulation and cytokines driving the SpA syndrome, including IL\u201017\/IL\u201022\u2013dependent enthesitis. Innate IL\u201022 production promotes ileal tolerance.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.38638","type":"journal-article","created":{"date-parts":[[2014,3,24]],"date-time":"2014-03-24T23:16:23Z","timestamp":1395702983000},"page":"1755-1767","source":"Crossref","is-referenced-by-count":202,"title":["Interleukin\u201023 Mediates the Intestinal Response to Microbial \u03b2\u20101,3\u2010Glucan and the Development of Spondyloarthritis Pathology in SKG Mice"],"prefix":"10.1002","volume":"66","author":[{"given":"Helen","family":"Benham","sequence":"first","affiliation":[{"name":"University of Queensland and Princess Alexandra Hospital Brisbane, Queensland Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda M.","family":"Rehaume","sequence":"additional","affiliation":[{"name":"University of Queensland and Princess Alexandra Hospital Brisbane, Queensland Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sumaira 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