{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:38:32Z","timestamp":1790401112970,"version":"4.1.0"},"reference-count":27,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,9,9]],"date-time":"2015-09-09T00:00:00Z","timestamp":1441756800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81301792"],"award-info":[{"award-number":["81301792"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Interleukin\u201017 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017) is a cytokine with critical functions in multiple autoimmune diseases. However, its roles in type I diabetes and the underlying mechanisms remain to be fully elucidated. In the current study, we investigated the impact of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 deficiency on streptozotocin (<jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>) \u2010induced diabetes. <jats:italic>Il\u201017<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice exhibited attenuated hyperglycaemia and insulitis after <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content> treatment compared with control mice. The <jats:italic>Il\u201017<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice had fewer <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> cells infiltrating the pancreas than wild\u2010type controls after <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content> injection. Wild\u2010type mice showed increased percentage and number of splenic <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> cells and decreased Gr1<jats:sup>+<\/jats:sup>\u00a0<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>11b<jats:sup>+<\/jats:sup> myeloid\u2010derived suppressor cells (<jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content>) after <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content> treatment, but <jats:italic>Il\u201017<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice maintained the percentages and numbers of splenic <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> cells and <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content>, suggesting that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 is implicated in <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>\u2010induced cellular immune responses in the spleen. We further purified the <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> from spleens of <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>\u2010treated mice. <jats:italic>Il\u201017<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> showed increased ability to suppress <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> cell proliferation <jats:italic>in\u00a0vitro<\/jats:italic> compared with wild\u2010type <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content>. Transfer of <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> to diabetic mice showed that <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> from <jats:italic>Il\u201017<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice could ameliorate hyperglycaemia. Moreover, recipients with <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> from <jats:italic>Il\u201017<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice had a decreased percentage of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> cell in the spleen compared with recipients with <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> from wild\u2010type mice. These data suggest that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 is required in splenic <jats:styled-content style=\"fixed-case\">MDSC<\/jats:styled-content> function after <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content> delivery. In summary, our study has revealed a pathogenic role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 in an <jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>\u2010induced diabetes model with important implications for our understanding of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 function in autoimmune diseases.<\/jats:p>","DOI":"10.1111\/imm.12512","type":"journal-article","created":{"date-parts":[[2015,7,25]],"date-time":"2015-07-25T15:08:50Z","timestamp":1437836930000},"page":"339-346","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Interleukin\u201017A deficiency ameliorates streptozotocin\u2010induced diabetes"],"prefix":"10.1111","volume":"146","author":[{"given":"Zan","family":"Tong","sequence":"first","affiliation":[{"name":"School of Basic Medical Sciences Wuhan University Wuha 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