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This study was to explore a novel anti\u2010inflammatory role and cellular\/molecular mechanism of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201027 in allergic inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A murine model of experimental allergic conjunctivitis (<jats:styled-content style=\"fixed-case\">EAC<\/jats:styled-content>) was induced in <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c, C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 or <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201027R\u03b1\u2010deficient (<jats:italic><jats:styled-content style=\"fixed-case\">WSX<\/jats:styled-content>\u20101<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) mice by short ragweed pollen, with untreated or <jats:styled-content style=\"fixed-case\">PBS<\/jats:styled-content>\u2010treated mice as controls. The serum, eyeballs, conjunctiva, cervical lymph nodes (<jats:styled-content style=\"fixed-case\">CLN<\/jats:styled-content>s) were used for study. Gene expression was determined by <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">qPCR<\/jats:styled-content>, and protein production and activation were evaluated by immunostaining, <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content> and Western blotting.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Typical allergic manifestations and stimulated thymic stromal lymphopoietin (<jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content>) signaling and Th2 responses were observed in ocular surface of <jats:styled-content style=\"fixed-case\">EAC<\/jats:styled-content> models in <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c and C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 mice. The decrease of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201027 at <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201027\/<jats:styled-content style=\"fixed-case\">EBI<\/jats:styled-content>3) and protein levels were detected in serum, conjunctiva and <jats:styled-content style=\"fixed-case\">CLN<\/jats:styled-content>, as evaluated by <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">qPCR<\/jats:styled-content>, immunofluorescent staining, <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content> and Western blotting. <jats:styled-content style=\"fixed-case\">EAC<\/jats:styled-content> induced in <jats:italic><jats:styled-content style=\"fixed-case\">WSX<\/jats:styled-content>\u20101<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice showed aggravated allergic signs with higher <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content>\u2010driven Th2\u2010dominant inflammation, accompanied by stimulated Th17 responses, including <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F, and transcription factor <jats:styled-content style=\"fixed-case\">ROR<\/jats:styled-content>\u03b3t. In contrast, Th1 cytokine <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u03b3 and Treg marker <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010, with their respective transcription factors T\u2010bet and foxp3, were largely suppressed. Interestingly, imbalanced activation between reduced phosphor (P)\u2010<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>1 and stimulated P\u2010<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>6 were revealed in <jats:styled-content style=\"fixed-case\">EAC<\/jats:styled-content>, especially <jats:italic><jats:styled-content style=\"fixed-case\">WSX<\/jats:styled-content>\u20101<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>\u2010<jats:styled-content style=\"fixed-case\">EAC<\/jats:styled-content> mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These findings demonstrated a natural protective mechanism by <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201027, of which signaling deficiency develops a Th17\u2010type hyperresponse that further aggravates Th2\u2010dominant allergic inflammation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.13691","type":"journal-article","created":{"date-parts":[[2018,12,5]],"date-time":"2018-12-05T06:05:01Z","timestamp":1543989901000},"page":"910-921","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["<scp>IL<\/scp>\u201027 signaling deficiency develops Th17\u2010enhanced Th2\u2010dominant inflammation in murine allergic conjunctivitis model"],"prefix":"10.1111","volume":"74","author":[{"given":"Xin","family":"Chen","sequence":"first","affiliation":[{"name":"School of Optometry and Ophthalmology Wenzhou Medical University Wenzhou China"},{"name":"Ocular Surface Center Cullen Eye Institute Department of Ophthalmology Baylor College of Medicine Houston Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruzhi","family":"Deng","sequence":"additional","affiliation":[{"name":"School of Optometry and Ophthalmology Wenzhou Medical University Wenzhou 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