{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T02:32:52Z","timestamp":1791340372430,"version":"4.3.1"},"reference-count":41,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,3,30]],"date-time":"2009-03-30T00:00:00Z","timestamp":1238371200000},"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; Rheumatism"],"published-print":{"date-parts":[[2009,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Subclinical gut inflammation is common in spondylarthritis, but the immunologic abnormalities underlying this process are undefined. Perturbation of the interleukin\u201023 (IL\u201023)\/Th17 axis has emerged as a fundamental trigger of chronic inflammation. This study was undertaken to investigate the expression and tissue distribution of IL\u201023\/Th17\u2013related molecules in Crohn's disease (CD) and in subclinical gut inflammation in ankylosing spondylitis (AS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Quantitative gene expression analysis of Th1\/Th2 and IL\u201023\/Th17 responses was performed in intestinal biopsy samples obtained from 12 patients with CD, 15 patients with AS, and 13 controls. IL\u201023 tissue distribution and identification of IL\u201023\u2013producing cells were evaluated by immunohistochemistry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We demonstrated a strong and significant up\u2010regulation of IL\u201023p19 transcripts in the terminal ileum in patients with AS and patients with CD. IL\u201023 was abundantly produced by infiltrating monocyte\u2010like cells in inflamed mucosa from AS and CD patients. Notably, we also identified Paneth cells as a major source of IL\u201023 in patients with AS, patients with CD, and normal controls. Unlike CD, in AS patients, IL\u201023 was not associated with up\u2010regulation of IL\u201017 and the IL\u201017\u2013inducing cytokines IL\u20106 and IL\u20101\u03b2. Finally, while the Th1\u2010related cytokines interferon\u2010\u03b3, IL\u201012p35, and IL\u201027p28 were overexpressed only in CD patients, IL\u20104, IL\u20105, and STAT\u20106 were also significantly increased in AS patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings indicate that overexpression of IL\u201023, but not IL\u201017, is a pivotal feature of subclinical gut inflammation in AS. Identification of resident Paneth cells as a pivotal source of IL\u201023 in physiologic and pathologic conditions strongly suggests that IL\u201023 is a master regulator of gut mucosal immunity, providing a pathophysiologic significance to the reported association between IL\u201023 receptor polymorphisms and intestinal inflammation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.24389","type":"journal-article","created":{"date-parts":[[2009,3,30]],"date-time":"2009-03-30T21:45:08Z","timestamp":1238449508000},"page":"955-965","source":"Crossref","is-referenced-by-count":214,"title":["Overexpression of interleukin\u201023, but not interleukin\u201017, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis"],"prefix":"10.1002","volume":"60","author":[{"given":"Francesco","family":"Ciccia","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michele","family":"Bombardieri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alfonso","family":"Principato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"AnnaRita","family":"Giardina","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudio","family":"Tripodo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rossana","family":"Porcasi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergio","family":"Peralta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vito","family":"Franco","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ennio","family":"Giardina","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio","family":"Craxi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Costantino","family":"Pitzalis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giovanni","family":"Triolo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,3,30]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/XXVII.suppl_2.95"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1053\/gast.1996.v110.pm8964393"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.berh.2006.03.010"},{"key":"e_1_2_6_5_2","doi-asserted-by":"crossref","first-page":"6276","DOI":"10.4049\/jimmunol.159.12.6276","article-title":"A 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