{"created":"2023-06-26T11:00:05.523375+00:00","id":288,"links":{},"metadata":{"_buckets":{"deposit":"68e1e306-21bb-42db-b893-cee458ab2bd1"},"_deposit":{"created_by":26,"id":"288","owners":[26],"pid":{"revision_id":0,"type":"depid","value":"288"},"status":"published"},"_oai":{"id":"oai:oist.repo.nii.ac.jp:00000288","sets":["6:165","6:33"]},"author_link":["943","939","944","941","938","936","937","942","940"],"item_10001_biblio_info_7":{"attribute_name":"Bibliographic Information","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2017-05-30","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"15628","bibliographicVolumeNumber":"8","bibliographic_titles":[{},{"bibliographic_title":"Nature Communications","bibliographic_titleLang":"en"}]}]},"item_10001_creator_3":{"attribute_name":"Author","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Hasan, Zafrul"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Koizumi, Shin-ichi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Sasaki, Daiki"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Yamada, Hayato"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Arakaki, Nana"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Fujihara, Yoshitaka"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Okitsu, Shiho"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Shirahata, Hiroki"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Ishikawa, Hiroki"}],"nameIdentifiers":[{}]}]},"item_10001_description_5":{"attribute_name":"Abstract","attribute_value_mlt":[{"subitem_description":"CD4+ T-helper cells producing interleukin-17 (IL-17), known as T-helper 17 (TH17) cells, comprise heterogeneous subsets that exhibit distinct pathogenicity. Although pathogenic and non-pathogenic TH17 subsets share a common RORγt-dependent TH17 transcriptional programme, transcriptional regulatory mechanisms specific to each of these subsets are mostly unknown. Here we show that the AP-1 transcription factor JunB is critical for TH17 pathogenicity. JunB, which is induced by IL-6, is essential for expression of RORγt and IL-23 receptor by facilitating DNA binding of BATF at the Rorc locus in IL-23-dependent pathogenic TH17 cells, but not in TGF-β1-dependent non-pathogenic TH17 cells. Junb-deficient T cells fail to induce TH17-mediated autoimmune encephalomyelitis and colitis. However, JunB deficiency does not affect the abundance of gut-resident non-pathogenic TH17 cells. The selective requirement of JunB for IL-23-dependent TH17 pathogenicity suggests that the JunB-dependent pathway may be a therapeutic target for autoimmune diseases.","subitem_description_type":"Other"}]},"item_10001_publisher_8":{"attribute_name":"Publisher","attribute_value_mlt":[{"subitem_publisher":"Springer Nature"}]},"item_10001_relation_13":{"attribute_name":"PubMedNo.","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"info:pmid/28555647","subitem_relation_type_select":"PMID"}}]},"item_10001_relation_14":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"info:doi/10.1038/ncomms15628","subitem_relation_type_select":"DOI"}}]},"item_10001_relation_17":{"attribute_name":"Related site","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://www.nature.com/articles/ncomms15628#abstract","subitem_relation_type_select":"URI"}}]},"item_10001_rights_15":{"attribute_name":"Rights","attribute_value_mlt":[{"subitem_rights":"© 2017 The Author(s) "}]},"item_10001_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"2041-1723","subitem_source_identifier_type":"ISSN"}]},"item_10001_version_type_20":{"attribute_name":"Author's flag","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-02-27"}],"displaytype":"detail","filename":"ncomms15628.pdf","filesize":[{"value":"1.2 MB"}],"format":"application/pdf","license_note":"Creative Commons Attribution 4.0 International  \n(http://creativecommons.org/licenses/by/4.0/)\n","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"ncomms15628","url":"https://oist.repo.nii.ac.jp/record/288/files/ncomms15628.pdf"},"version_id":"6b4879c9-468e-4525-b60f-315586f11cf1"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"JunB is essential for IL-23-dependent pathogenicity of Th17 cells","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"JunB is essential for IL-23-dependent pathogenicity of Th17 cells","subitem_title_language":"en"}]},"item_type_id":"10001","owner":"26","path":["33","165"],"pubdate":{"attribute_name":"公開日","attribute_value":"2018-02-27"},"publish_date":"2018-02-27","publish_status":"0","recid":"288","relation_version_is_last":true,"title":["JunB is essential for IL-23-dependent pathogenicity of Th17 cells"],"weko_creator_id":"26","weko_shared_id":26},"updated":"2023-06-26T12:06:23.201933+00:00"}