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However, deficiency of <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010<jats:italic>\u03b3<\/jats:italic>, a signature Th1 cytokine, aggravated <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content>, with features of elevated production of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A, despite an alleviated systemic Th1 immune response. We hypothesized that Th17 cells and their cytokines might play a pathogenic role in <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content>. To further clarify the roles of these Th and regulatory T cell (Treg) cytokines in the pathogenesis of <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content> and their interrelationship, we investigated the expression of Th1\/Th2\/Th17\/Treg cytokines in <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content> in this study. We found that the levels of Th17 cells and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A in cauda equina (<jats:styled-content style=\"fixed-case\">CE<\/jats:styled-content>)\u2010infiltrating cells and splenic mononuclear cells (<jats:styled-content style=\"fixed-case\">MNC<\/jats:styled-content>s) as well as in serum paralleled the disease evolution, which increased progressively during the initiation stage and reached higher value at the peak of <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content>. The same pattern was also noticed for the expression of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201022. The diverse expression profiles of FoxP3, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 receptors A and C were seen in <jats:styled-content style=\"fixed-case\">CE<\/jats:styled-content>\u2010infiltrating cells and splenic <jats:styled-content style=\"fixed-case\">MNC<\/jats:styled-content>s in <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content>. These findings indicate a major pro\u2010inflammatory role of Th17 cells and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A in the pathogenesis of <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content>. Therapeutic interventions may be focused upon inhibiting Th17 cells and their cytokines in the early phase of <jats:styled-content style=\"fixed-case\">EAN<\/jats:styled-content>, so as to delay and suppress clinical signs of the disease, which has relevance for future studies on pathogenesis and treatment of <jats:styled-content style=\"fixed-case\">GBS<\/jats:styled-content> in humans.<\/jats:p>","DOI":"10.1111\/sji.12201","type":"journal-article","created":{"date-parts":[[2014,6,9]],"date-time":"2014-06-09T10:48:03Z","timestamp":1402310883000},"page":"180-190","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Mitigated Tregs and Augmented Th17 Cells and Cytokines are Associated with Severity of Experimental Autoimmune Neuritis"],"prefix":"10.1111","volume":"80","author":[{"given":"X.","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Neurology the First Hospital of Jilin University 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