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However, there is an ongoing debate regarding the reverse plasticity (conversion from Th1 to Th17). We show here that ectopic ROR\u2010\u03b3t expression can restore or initiate IL\u201017 expression by non\u2010classic or classic Th1 cells, respectively, while common pro\u2010Th17 cytokine cocktails are ineffective. This stability of the Th1 phenotype is at least partially due to the presence of a molecular machinery governed by the transcription factor Eomes, which promotes IFN\u2010\u03b3 secretion while inhibiting the expression of ROR\u2010\u03b3t and IL\u201017. By using a mouse model of T\u00a0cell\u2010dependent colitis we demonstrate that Eomes controls non\u2010classic Th1 cell development also in vivo and promotes their pathogenic potential. Eomes expression associates to a highly inflammatory phenotype also in patients with juvenile idiopathic arthritis. Indeed, it favors the acquisition of a cytotoxic signature, and promotes the development of IFN\u2010\u03b3<jats:sup>+<\/jats:sup>GM\u2010CSF<jats:sup>+<\/jats:sup> cells that have been described to be pathogenic in chronic inflammatory disorders.<\/jats:p>","DOI":"10.1002\/eji.201847677","type":"journal-article","created":{"date-parts":[[2018,8,24]],"date-time":"2018-08-24T14:25:49Z","timestamp":1535120749000},"page":"79-95","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":77,"title":["<i>Eomes<\/i> controls the development of Th17\u2010derived (non\u2010classic) Th1 cells during chronic inflammation"],"prefix":"10.1002","volume":"49","author":[{"given":"Alessio","family":"Mazzoni","sequence":"first","affiliation":[{"name":"Department of Experimental and Clinical Medicine and DENOTHE Center University of Florence  Firenze 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