{"created":"2023-05-15T16:32:28.345155+00:00","id":4329,"links":{},"metadata":{"_buckets":{"deposit":"716f5ea2-6530-4403-b5f5-7860f5f983a6"},"_deposit":{"created_by":6,"id":"4329","owners":[6],"pid":{"revision_id":0,"type":"depid","value":"4329"},"status":"published"},"_oai":{"id":"oai:nagasaki-u.repo.nii.ac.jp:00004329","sets":["10:22:24"]},"author_link":["114831","114830"],"item_5_alternative_title_19":{"attribute_name":"その他のタイトル","attribute_value_mlt":[{"subitem_alternative_title":"IL-17/IFN-γ受容体遺伝子ダブル欠損NODマウスにおける糖尿病発症抑制"}]},"item_5_biblio_info_6":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2013-10-02","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"8","bibliographicPageEnd":"1780","bibliographicPageStart":"1773","bibliographicVolumeNumber":"56","bibliographic_titles":[{"bibliographic_title":"Diabetologia"}]}]},"item_5_date_granted_64":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"2013-10-02"}]},"item_5_degree_grantor_62":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_name":"Nagasaki University (長崎大学)"}],"subitem_degreegrantor_identifier":[{"subitem_degreegrantor_identifier_name":"17301","subitem_degreegrantor_identifier_scheme":"kakenhi"}]}]},"item_5_degree_name_61":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"博士(医学)"}]},"item_5_description_4":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Aims/hypothesis\nT helper type (Th) 17 cells have been shown to play important roles in mouse models of several autoimmune diseases that have been classified as Th1 diseases. In the NOD mouse, the relevance of Th1 and Th17 is controversial, because single-cytokine-deficient NOD mice develop diabetes similarly to wild-type NOD mice.\nMethods\nWe studied the impact of IL-17/IFN-γ receptor double deficiency in NOD mice on the development of insulitis/diabetes compared with IL-17 single-deficient mice and wild-type mice by monitoring diabetes-related phenotypes. The lymphocyte phenotypes were determined by flow cytometric analysis.\nResults\nIL-17 single-deficient NOD mice showed delayed onset of diabetes and reduced severity of insulitis, but the cumulative incidence of longstanding diabetes in the IL-17-deficient mice was similar to that in wild-type mice. The IL-17/IFN-γ receptor double-deficient NOD mice showed an apparent decline in longstanding diabetes onset, but not in insulitis compared with that in the IL-17 single-deficient mice. We also found that double-deficient NOD mice had a severe lymphopenic phenotype and preferential increase in regulatory T cells among CD4+ T cells compared with the IL-17 single-deficient mice and wild-type NOD mice. An adoptive transfer study with CD4+CD25? T cells from young non-diabetic IL-17 single-deficient NOD mice, but not those from older mice, showed significantly delayed disease onset in immune-deficient hosts compared with the corresponding wild-type mice.\nConclusions/interpretation\nThese results indicate that IL-17/Th17 participates in the development of insulitis and that both IL-17 and IFN-γ signalling may synergistically contribute to the development of diabetes in NOD mice.","subitem_description_type":"Abstract"}]},"item_5_description_5":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"長崎大学学位論文 学位記番号:博(医歯薬)甲第630号 学位授与年月日:平成25年10月2日","subitem_description_type":"Other"},{"subitem_description":"Author：G. Kuriya, T. Uchida, S. Akazawa, M. Kobayashi, K. Nakamura, T. Satoh, I. Horie, E. Kawasaki, H. Yamasaki, L. Yu, Y. Iwakura, H. Sasaki, Y. Nagayama, A. Kawakami, N. Abiru","subitem_description_type":"Other"},{"subitem_description":"Citation: Diabetologia, 56(8), pp.1773-1780; 2013","subitem_description_type":"Other"}]},"item_5_description_69":{"attribute_name":"引用","attribute_value_mlt":[{"subitem_description":"Nagasaki University (長崎大学), 博士(医学) (2013-10-02)","subitem_description_type":"Other"}]},"item_5_dissertation_number_65":{"attribute_name":"学位授与番号","attribute_value_mlt":[{"subitem_dissertationnumber":"甲医歯薬第630号"}]},"item_5_full_name_3":{"attribute_name":"著者別名","attribute_value_mlt":[{"nameIdentifiers":[{"nameIdentifier":"114831","nameIdentifierScheme":"WEKO"}],"names":[{"name":"Kuriya, Genpei"}]}]},"item_5_publisher_33":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Springer-Verlag Berlin Heidelberg"}]},"item_5_relation_12":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1007/s00125-013-2935-8","subitem_relation_type_select":"DOI"}}]},"item_5_relation_42":{"attribute_name":"関係URI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://hdl.handle.net/10069/34140","subitem_relation_type_select":"HDL"}}]},"item_5_rights_13":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"c Springer-Verlag Berlin Heidelberg 2013"},{"subitem_rights":"The final publication is available at link.springer.com"}]},"item_5_source_id_7":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0012186X","subitem_source_identifier_type":"ISSN"}]},"item_5_source_id_8":{"attribute_name":"EISSN","attribute_value_mlt":[{"subitem_source_identifier":"14320428","subitem_source_identifier_type":"ISSN"}]},"item_5_text_67":{"attribute_name":"学位の種類","attribute_value_mlt":[{"subitem_text_value":"課程博士"}]},"item_5_version_type_16":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_access_right":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open access","subitem_access_right_uri":"http://purl.org/coar/access_right/c_abf2"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"厨, 源平"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2021-02-01"}],"displaytype":"detail","filename":"SupplFig.pdf","filesize":[{"value":"107.7 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"SupplFig.pdf","objectType":"fulltext","url":"https://nagasaki-u.repo.nii.ac.jp/record/4329/files/SupplFig.pdf"},"version_id":"07728b90-589a-485f-8bd9-0db7b7ff0f57"},{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2021-02-01"}],"displaytype":"detail","filename":"ISYK630_Kuriya.pdf","filesize":[{"value":"1.4 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"ISYK630_Kuriya.pdf","objectType":"fulltext","url":"https://nagasaki-u.repo.nii.ac.jp/record/4329/files/ISYK630_Kuriya.pdf"},"version_id":"4c8cfc82-d14b-4d1c-853e-713dcbd2a280"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"IL-17","subitem_subject_scheme":"Other"},{"subitem_subject":"IFN-γ","subitem_subject_scheme":"Other"},{"subitem_subject":"NOD mice","subitem_subject_scheme":"Other"},{"subitem_subject":"type 1 diabetes","subitem_subject_scheme":"Other"},{"subitem_subject":"Th17","subitem_subject_scheme":"Other"},{"subitem_subject":"lymphopenia","subitem_subject_scheme":"Other"}]},"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":"doctoral thesis","resourceuri":"http://purl.org/coar/resource_type/c_db06"}]},"item_title":"Double deficiency in IL-17 and IFN-γ signalling significantly suppresses the development of diabetes in the NOD mouse","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Double deficiency in IL-17 and IFN-γ signalling significantly suppresses the development of diabetes in the NOD mouse","subitem_title_language":"en"}]},"item_type_id":"5","owner":"6","path":["24"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2015-06-05"},"publish_date":"2015-06-05","publish_status":"0","recid":"4329","relation_version_is_last":true,"title":["Double deficiency in IL-17 and IFN-γ signalling significantly suppresses the development of diabetes in the NOD mouse"],"weko_creator_id":"6","weko_shared_id":-1},"updated":"2023-08-23T05:02:56.475038+00:00"}