The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote TH17 cell–dependent emphysema

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dc.citation.firstpage1185en_US
dc.citation.journalTitleNature Immunologyen_US
dc.citation.lastpage1194en_US
dc.citation.volumeNumber16en_US
dc.contributor.authorLu, Wenen_US
dc.contributor.authorYou, Ranen_US
dc.contributor.authorYuan, Xiaoyien_US
dc.contributor.authorYang, Tianshuen_US
dc.contributor.authorSamuel, Errol L.G.en_US
dc.contributor.authorMarcano, Daniela C.en_US
dc.contributor.authorSikkema, William K.A.en_US
dc.contributor.authorTour, James M.en_US
dc.contributor.authorRodriguez, Antonyen_US
dc.contributor.authorKheradmand, Farrahen_US
dc.contributor.authorCorry, David B.en_US
dc.date.accessioned2016-06-27T15:39:57Zen_US
dc.date.available2016-06-27T15:39:57Zen_US
dc.date.issued2015en_US
dc.description.abstractSmoking-related emphysema is a chronic inflammatory disease driven by the T(H)17 subset of helper T cells through molecular mechanisms that remain obscure. Here we explored the role of the microRNA miR-22 in emphysema. We found that miR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism that involved the transcription factor NF-κB. Mice deficient in miR-22, but not wild-type mice, showed attenuated T(H)17 responses and failed to develop emphysema after exposure to smoke or nCB. We further found that miR-22 controlled the activation of APCs and T(H)17 responses through the activation of AP-1 transcription factor complexes and the histone deacetylase HDAC4. Thus, miR-22 is a critical regulator of both emphysema and T(H)17 responses.en_US
dc.identifier.citationLu, Wen, You, Ran, Yuan, Xiaoyi, et al.. "The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote TH17 cell–dependent emphysema." <i>Nature Immunology,</i> 16, (2015) Nature Publishing Group: 1185-1194. http://dx.doi.org/10.1038/ni.3292.en_US
dc.identifier.doihttp://dx.doi.org/10.1038/ni.3292en_US
dc.identifier.urihttps://hdl.handle.net/1911/90576en_US
dc.language.isoengen_US
dc.publisherNature Publishing Groupen_US
dc.rightsThis is an author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by the Nature Publishing Group.en_US
dc.titleThe microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote TH17 cell–dependent emphysemaen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpost-printen_US
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