{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T12:08:53Z","timestamp":1792843733526,"version":"4.5.0"},"reference-count":196,"publisher":"BMJ","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2009,8]]},"abstract":"<jats:p>\n                    Traditionally, Crohn\u2019s disease has been associated with a Th1 cytokine profile, while Th2 cytokines are modulators of ulcerative colitis. This concept has been challenged by the description of tolerising regulatory T cells (Treg) and by proinflammatory Th17 cells, a novel T cell population characterised by the master transcription factor ROR\u03b3t, the surface markers IL23R and CCR6, and by production of the proinflammatory cytokines IL17A, IL17F, IL21, IL22 and IL26, and the chemokine CCL20. Th17 cells differentiate under the influence of IL1\u03b2, IL6, IL21 and IL23. Recent studies indicate that TGF\u03b2 is essential not only for the development of murine Th17 cells but also for differentiation of human Th17 cells. TGF\u03b2 reciprocally regulates the differentiation of inflammatory Th17 cells and suppressive Treg subsets, with the concomitant presence of proinflammatory cytokines favouring Th17 cell differentiation. Several studies demonstrated an important role of Th17 cells in intestinal inflammation, particularly in Crohn\u2019s disease. Genome-wide association studies indicate that\n                    <jats:italic>IL23R<\/jats:italic>\n                    and five additional genes involved in Th17 differentiation (\n                    <jats:italic>IL12B<\/jats:italic>\n                    ,\n                    <jats:italic>JAK2<\/jats:italic>\n                    ,\n                    <jats:italic>STAT3<\/jats:italic>\n                    ,\n                    <jats:italic>CCR6<\/jats:italic>\n                    and\n                    <jats:italic>TNFSF15<\/jats:italic>\n                    ) are associated with susceptibility to Crohn\u2019s disease and partly also to ulcerative colitis. Taken together, both Th1 and Th17 cells are important mediators of inflammation in Crohn\u2019s disease, although activities previously ascribed to IL12 may be mediated by IL23. Anti-IL12\/IL23p40 antibody therapy, which targets both Th1 and Th17 cells, is effective in Crohn\u2019s disease. However, the complex relationship between Th1 and Th17 cells has not been completely analysed. This will be of great importance to delineate the specific contributions of these cells to Crohn\u2019s disease and other autoimmune diseases.\n                  <\/jats:p>","DOI":"10.1136\/gut.2008.163667","type":"journal-article","created":{"date-parts":[[2009,7,10]],"date-time":"2009-07-10T19:43:12Z","timestamp":1247254992000},"page":"1152-1167","source":"Crossref","is-referenced-by-count":584,"title":["Crohn\u2019s disease: Th1, Th17 or both? The change of a paradigm: new immunological and genetic insights implicate Th17 cells in the pathogenesis of Crohn\u2019s disease"],"prefix":"10.1136","volume":"58","author":[{"given":"S","family":"Brand","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2009,7,10]]},"reference":[{"key":"2025121300505609000_58.8.1152.1","doi-asserted-by":"publisher","DOI":"10.1038\/nature06005"},{"key":"2025121300505609000_58.8.1152.2","doi-asserted-by":"crossref","first-page":"2348","DOI":"10.4049\/jimmunol.136.7.2348","article-title":"Two types of murine helper T cell clone. I. 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