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However, whether <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>c17 cells are involved remains largely unknown. We investigated <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>c17 involvement using a cigarette smoke\u2010exposure model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Groups of mice were exposed to cigarette smoke or filtered air. At weeks 2, 8, 12 and 24, mice were sacrificed to observe histological changes by HE stain and\/or immunohistochemical staining. The frequency of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cell subsets in the lung and spleen were detected by flow cytometry. In addition, the expression levels of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cell\u2010related factors were measured by real\u2010time polymerase chain reaction or enzyme\u2010linked immunosorbent assay.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Cigarette smoke caused substantial inflammatory cell infiltration and led to emphysema. Cigarette smoke exposure promoted the expression of interferon\u2010gamma (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>)\u2010\u03b3 and interleukin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>)\u201017<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> at the messenger ribonucleic acid and protein levels. In addition to <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>c1 and <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h17 cells, pulmonary and splenic <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>c17 cells increased, which was accompanied by the upregulation of cytokines <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, transforming growth factor beta (<jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>)\u2010\u03b2) and transcriptional factors <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>tat3 and RAR\u2010related orphan receptor gamma. Compared with untreated mice, \u03b3<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AX<\/jats:styled-content>\u2010positive cells were more frequently observed in mice exposed to cigarette smoke.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Long\u2010term cigarette smoke exposure induced <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>c17 cell expansion both locally and distally, which was associated with emphysema and deoxyribonucleic acid damage. As an important source of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>, this <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cell subset may be a potential target for chronic obstructive pulmonary disease therapy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/resp.12486","type":"journal-article","created":{"date-parts":[[2015,2,13]],"date-time":"2015-02-13T07:25:22Z","timestamp":1423812322000},"page":"426-433","source":"Crossref","is-referenced-by-count":38,"title":["<scp>T<\/scp>c17 cells are associated with cigarette smoke\u2010induced lung inflammation and emphysema"],"prefix":"10.1111","volume":"20","author":[{"given":"Hongbin","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine Second Hospital of Zhejiang University School of Medicine  Hangzhou Zhejiang 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