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To investigate the role of gp130 under inflammatory conditions, T\u2010cell\u2010specific conditional gp130 mice were first bred to the IL\u201010\u2010deficient background and were then infected with the gastrointestinal nematode <jats:italic>Trichuris muris<\/jats:italic>. While IL\u201010<jats:sup>\u2212\/\u2212<\/jats:sup> mice were highly susceptible to <jats:italic>T. muris<\/jats:italic>, developed a mixed Th1\/Th17 response and displayed severe inflammation of the caecum, infection of mice with an additional T\u2010cell\u2010specific deletion of gp130 signalling completely reversed the phenotype. These mice showed an accelerated worm expulsion that was associated with the rapid generation of a strong Th2 immune response and a significant increase in Foxp3\u2010expressing Treg. Therefore, gp130 signalling in T cells regulates a switch between proinflammatory and pathogenic Th1\/Th17 cells and regulatory Th2\/Treg <jats:italic>in vivo<\/jats:italic>. Taken together, the data demonstrate that gp130 signalling in T cells is a positive regulator of inflammatory processes, favouring the Th1\/Th17 axis.<\/jats:p>","DOI":"10.1002\/eji.200838710","type":"journal-article","created":{"date-parts":[[2009,7,10]],"date-time":"2009-07-10T22:07:07Z","timestamp":1247263627000},"page":"2173-2183","source":"Crossref","is-referenced-by-count":18,"title":["T\u2010cell\u2010specific deletion of gp130 renders the highly susceptible IL\u201010\u2010deficient mouse resistant to intestinal nematode infection"],"prefix":"10.1002","volume":"39","author":[{"given":"Nicolas","family":"Fasnacht","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marina 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