{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T01:06:12Z","timestamp":1791421572093,"version":"4.3.3"},"reference-count":43,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:00:00Z","timestamp":1339459200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2012,7]]},"abstract":"Interleukin (IL<\/jats:styled-content>)\u201033, a member of the IL<\/jats:styled-content>\u20101 cytokine family, is an important modulator of the immune system associated with several immune\u2010mediated disorders. High levels of IL<\/jats:styled-content>\u201033 are expressed by the central nervous system (CNS<\/jats:styled-content>) suggesting a potential role of IL<\/jats:styled-content>\u201033 in autoimmune CNS<\/jats:styled-content> diseases. We have investigated the expression and function of IL<\/jats:styled-content>\u201033 in the development of experimental autoimmune encephalomyelitis (EAE<\/jats:styled-content>) in mice. We report here that IL<\/jats:styled-content>\u201033 and its receptor ST<\/jats:styled-content>2 (IL<\/jats:styled-content>\u201033R<\/jats:styled-content>\u03b1) are highly expressed in spinal cord tissue, and ST<\/jats:styled-content>2 expression is markedly increased in the spinal cords of mice with EAE<\/jats:styled-content>. Furthermore, ST<\/jats:styled-content>2\u2010deficient (ST<\/jats:styled-content>2\u2212\/\u2212<\/jats:sup>) mice developed exacerbated EAE<\/jats:styled-content> compared with wild\u2010type (WT<\/jats:styled-content>) mice while WT<\/jats:styled-content>, but not ST<\/jats:styled-content>2\u2212\/\u2212<\/jats:sup> EAE<\/jats:styled-content> mice treated with IL<\/jats:styled-content>\u201033 developed significantly attenuated disease. IL<\/jats:styled-content>\u201033\u2010treated mice had reduced levels of IL<\/jats:styled-content>\u201017 and IFN<\/jats:styled-content>\u2010\u03b3 but produced increased amounts of IL<\/jats:styled-content>\u20105 and IL<\/jats:styled-content>\u201013. Lymph node and splenic macrophages of IL<\/jats:styled-content>\u201033\u2010treated mice showed polarization toward an alternatively activated macrophage (M<\/jats:styled-content>2) phenotype with significantly increased frequency of MR<\/jats:styled-content>+<\/jats:sup>PD<\/jats:styled-content>\u2010L<\/jats:styled-content>2+<\/jats:sup> cells. Importantly, adoptive transfer of these IL<\/jats:styled-content>\u201033\u2010treated macrophages attenuated EAE<\/jats:styled-content> development. Our data therefore demonstrate that IL<\/jats:styled-content>\u201033 plays a therapeutic role in autoimmune CNS<\/jats:styled-content> disease by switching a predominantly pathogenic Th17\/Th1 response to Th2 activity, and by polarization of anti\u2010inflammatory M<\/jats:styled-content>2 macrophages.<\/jats:p>","DOI":"10.1002\/eji.201141947","type":"journal-article","created":{"date-parts":[[2012,5,14]],"date-time":"2012-05-14T12:52:52Z","timestamp":1336999972000},"page":"1804-1814","source":"Crossref","is-referenced-by-count":292,"title":["IL<\/scp>\u201033 attenuates EAE by suppressing IL<\/scp>\u201017 and IFN<\/scp>\u2010\u03b3 production and inducing alternatively activated macrophages"],"prefix":"10.1002","volume":"42","author":[{"given":"Hui\u2010Rong","family":"Jiang","sequence":"first","affiliation":[{"name":"Strathclyde Institute of Pharmacy and Biomedical Sciences University of Strathclyde Glasgow 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