{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T02:08:30Z","timestamp":1791079710651,"version":"4.1.0"},"reference-count":18,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2008,10,1]],"date-time":"2008-10-01T00:00:00Z","timestamp":1222819200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>IL-23 has been implicated in the pathogenesis of several tissue-specific autoimmune diseases. Currently, celiac disease (CD) is the only autoimmune disease in which both the major genetic (95% HLA-DQ2+) and etiologic factors (dietary glutens) for susceptibility are known. We demonstrate that wheat gliadin induces significantly greater production of IL-23, IL-1\u03b2, and TNF-\u03b1 in PBMC from CD patients compared with HLA-DQ2+ healthy controls, strongly advocating a role for IL-23 in the pathogenesis of CD. Moreover, IL-1\u03b2 alone triggered IL-23 secretion and the IL-1R antagonist inhibited this response in PBMC and purified monocytes. This sequence of events was replicated by \u03b2-glucan, another substance known to induce IL-23 production. Our results suggest that gliadin and \u03b2-glucan stimulate IL-23 secretion through induction of the IL-1 signaling pathway and reveal for the first time that the IL-1 system regulates IL-23 production. These findings may provide therapeutic targets for this disease and other inflammatory conditions mediated by IL-23.<\/jats:p>","DOI":"10.4049\/jimmunol.181.7.4457","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T23:07:10Z","timestamp":1397862430000},"page":"4457-4460","source":"Crossref","is-referenced-by-count":58,"title":["Cutting Edge: IL-1 Controls the IL-23 Response Induced by Gliadin, the Etiologic Agent in Celiac Disease"],"prefix":"10.1093","volume":"181","author":[{"given":"Kristina M","family":"Harris","sequence":"first","affiliation":[{"name":"Pathology Department"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessio","family":"Fasano","sequence":"additional","affiliation":[{"name":"Mucosal Biology Research Center, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dean L","family":"Mann","sequence":"additional","affiliation":[{"name":"Pathology Department"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2008,10,1]]},"reference":[{"key":"2025032700302910700_R1","first-page":"2473","article-title":"Interleukin-23 drives innate and T cell-mediated intestinal inflammation","volume-title":"J. 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Gastroenterol.","year":"1998"},{"key":"2025032700302910700_R5","first-page":"2512","article-title":"Gliadin stimulation of murine macrophage inflammatory gene expression and intestinal permeability are MyD88-dependent: role of the innate immune response in celiac disease","volume-title":"J. Immunol.","year":"2006"},{"key":"2025032700302910700_R6","first-page":"30","article-title":"Association between innate response to gliadin and activation of pathogenic T cells in coeliac disease","volume-title":"Lancet","year":"2003"},{"key":"2025032700302910700_R7","first-page":"2226","article-title":"HLA-DQ2 and -DQ8 signatures of gluten T cell epitopes in celiac disease","volume-title":"J. Clin. Invest.","year":"2006"},{"key":"2025032700302910700_R8","first-page":"201","article-title":"Gliadin peptides activate blood monocytes from patients with celiac disease","volume-title":"J. Clin. 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IL-1 receptor antagonist inhibits IL-1-induced cytokine synthesis and blocks the binding of IL-1 to its type II receptor on human monocytes","volume-title":"Blood","year":"1992"},{"key":"2025032700302910700_R13","first-page":"4641","article-title":"IL-1\u03b2 causes an increase in intestinal epithelial tight junction permeability","volume-title":"J. Immunol.","year":"2007"},{"key":"2025032700302910700_R14","first-page":"428","article-title":"A unique dendritic cell subset accumulates in the celiac lesion and efficiently activates gluten-reactive T cells","volume-title":"Gastroenterology","year":"2006"},{"key":"2025032700302910700_R15","first-page":"2269","article-title":"Unique CD14 intestinal macrophages contribute to the pathogenesis of Crohn disease via IL-23\/IFN-\u03b3 axis","volume-title":"J. Clin. 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