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dc.contributor.authorXiao, Xiangen_US
dc.contributor.authorBalasubramanian, Savithrien_US
dc.contributor.authorLiu, Wentaoen_US
dc.contributor.authorChu, Xiufengen_US
dc.contributor.authorWang, Haibinen_US
dc.contributor.authorTaparowsky, Elizabeth J.en_US
dc.contributor.authorFu, Yang-Xinen_US
dc.contributor.authorChoi, Yongwonen_US
dc.contributor.authorWalsh, Matthew C.en_US
dc.contributor.authorLi, Xian Changen_US
dc.date.accessioned2014-03-10T20:34:01Z
dc.date.issued2012en_US
dc.identifier.citationXiao, Xiang, Savithri Balasubramanian, Wentao Liu, Xiufeng Chu, Haibin Wang, Elizabeth J. Taparowsky, Yang-Xin Fu, Yongwon Choi, Matthew C. Walsh, and Xian Chang Li. 2012. “OX40 signaling favors the induction of TH9 cells and airway inflammation.” Nature immunology 13 (10): 981-990. doi:10.1038/ni.2390. http://dx.doi.org/10.1038/ni.2390.en
dc.identifier.issn1529-2908en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:11878907
dc.description.abstractThe mechanisms regulating T helper 9 (TH9) cells and TH9-mediated diseases remain poorly defined. Here, we demonstrate that the receptor OX40 (Tnfrsf4) is a powerful inducer of TH9 cells in vitro and TH9-dependent airway inflammation in vivo. Under TGF-β based polarizing conditions, OX40 ligation eliminated production of induced regulatory T cells and TH17 cells, and divertedCD4+Foxp3− T cells to a TH9 phenotype. Mechanistically, OX40 activated the ubiquitin ligase TRAF6, which triggered the induction of NF-kB-inducing kinase (NIK) in CD4+ T cells and the non-canonical NF-kB pathway which subsequently lead toTH9 generation. Thus, our study identifies a previously unknown mechanism of TH9 induction and may have important clinical implications in allergic inflammation.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/ni.2390en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806044/pdf/en
dash.licenseLAAen_US
dc.titleOX40 signaling favors the induction of TH9 cells and airway inflammationen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalNature immunologyen
dash.depositing.authorWang, Haibinen_US
dc.date.available2014-03-10T20:34:01Z
dc.identifier.doi10.1038/ni.2390*
dash.contributor.affiliatedWang, Haibin


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