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It has recently emerged that a new class of T helper (Th) cells, defined by their ability to produce interleukin (IL)\u201017A (Th17), is associated with a host of inflammatory responses, including gastritis. However, the role of these Th17 cells in the pathogenesis of gastric cancer is less clear. To formally address this, we employed <jats:italic>gp130<\/jats:italic><jats:sup><jats:italic>F<\/jats:italic>\/<jats:italic>F<\/jats:italic><\/jats:sup> mice, which spontaneously develop gastric inflammation\u2010associated tumours akin to human intestinal\u2010type gastric cancer. At the molecular level, these tumours demonstrate hyper\u2010activation of the latent transcription factor signal transducer and activator of transcription (STAT)3 via the IL\u20106 cytokine family member, IL\u201011. In <jats:italic>gp130<\/jats:italic><jats:sup><jats:italic>F<\/jats:italic>\/<jats:italic>F<\/jats:italic><\/jats:sup> mice, the generation of Th17 cells, as well as the gastric expression of <jats:italic>IL\u201017a<\/jats:italic> and other Th17\u2010related factors (<jats:italic>Ror<\/jats:italic>\u03b3<jats:italic>t, IL\u201023<\/jats:italic>), were augmented compared to wild\u2010type <jats:italic>gp130<\/jats:italic><jats:sup>+\/+<\/jats:sup> mice. Consistent with a role for IL\u20106 and STAT3 in regulating IL\u201017A, increased Th17 generation and gastric expression of Th17\u2010related factors in <jats:italic>gp130<\/jats:italic><jats:sup><jats:italic>F<\/jats:italic>\/<jats:italic>F<\/jats:italic><\/jats:sup> mice were reduced to wild\u2010type levels in <jats:italic>gp130<\/jats:italic><jats:sup><jats:italic>F<\/jats:italic>\/<jats:italic>F<\/jats:italic><\/jats:sup><jats:italic>:Stat3<\/jats:italic><jats:sup>\u2212\/+<\/jats:sup> mice displaying normalized STAT3 activity, and also in <jats:italic>gp130<\/jats:italic><jats:sup><jats:italic>F<\/jats:italic>\/<jats:italic>F<\/jats:italic><\/jats:sup><jats:italic>:IL\u20106<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice. Importantly, genetic ablation of IL\u201017A in <jats:italic>gp130<\/jats:italic><jats:sup><jats:italic>F<\/jats:italic>\/<jats:italic>F<\/jats:italic><\/jats:sup>:<jats:italic>IL\u201017a<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice did not suppress the initiation and growth of gastric tumours. Furthermore, <jats:italic>IL\u201017A<\/jats:italic> and <jats:italic>RORC<\/jats:italic> gene expression was strongly increased in human gastric biopsies from patients with gastritis, but not gastric cancer. Collectively, our data suggest that increased expression of Th17\u2010related factors does not correlate with the molecular pathogenesis of gastric tumourigenesis. Copyright \u00a9 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.2933","type":"journal-article","created":{"date-parts":[[2011,5,10]],"date-time":"2011-05-10T07:46:51Z","timestamp":1305013611000},"page":"255-264","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["The molecular pathogenesis of STAT3\u2010driven gastric tumourigenesis in mice is independent of IL\u201017"],"prefix":"10.1002","volume":"225","author":[{"given":"Catherine L","family":"Kennedy","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Meri","family":"Najdovska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gareth 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