{"created":"2024-10-25T07:46:07.338053+00:00","id":2002889,"links":{},"metadata":{"_buckets":{"deposit":"865a2fc1-1c5c-43b2-a101-eceb6dc38e0e"},"_deposit":{"created_by":7,"id":"2002889","owners":[7],"pid":{"revision_id":0,"type":"depid","value":"2002889"},"status":"published"},"_oai":{"id":"oai:tokushima-u.repo.nii.ac.jp:02002889","sets":["1713853213384:1713853295607"]},"author_link":["174","1684","1648","1527"],"item_10001_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"1998-08","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"3","bibliographicPageEnd":"506","bibliographicPageStart":"499","bibliographicVolumeNumber":"102","bibliographic_titles":[{"bibliographic_title":"Journal of Clinical Investigation","bibliographic_titleLang":"en"}]}]},"item_10001_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Paracrine effect of transforming growth factor-β1 (TGF-β1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-β1 (pTGF-β1) in pancreatic islet (islet) α cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-β1). None of 27 NOD-RGP-TGF-β1 mice developed diabetes by 45 wk of age, in contrast to 40 and 71% in male and female nontransgenic mice, respectively. None of the NOD-RGP-TGF-β1 mice developed diabetes after cyclophosphamide (CY) administration. Adoptive transfer of splenocytes of NOD-RGP-TGF-β1 mice to neonatal NOD mice did not transfer diabetes after CY administration. Adoptive transfer of three types of diabetogenic lymphocytes to NOD-RGP-TGF-β1 and nontransgenic mice after CY administration led to the lower incidence of diabetes in NOD-RGP-TGF-β1 mice versus that in nontransgenic mice: 29 vs. 77% for diabetogenic splenocytes, 25 vs. 75% for islet β cell–specific Th1 clone cells, and 0 vs. 50% for islet β cell–specific CD8+ clone cells, respectively. Based on these, it is concluded that autoimmune diabetes in NOD mice is not a systemic disease and it can be completely prevented by the paracrine TGF-β1 in the islet compartment through protection against CD4+ and CD8+ effector lymphocytes.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10001_rights_15":{"attribute_name":"権利情報","attribute_value_mlt":[{"subitem_rights":"© The American Society for Clinical Investigation, Inc.","subitem_rights_language":"en"}]},"item_10001_source_id_9":{"attribute_name":"収録物ID","attribute_value_mlt":[{"subitem_source_identifier":"00219738","subitem_source_identifier_type":"ISSN"},{"subitem_source_identifier":"AA00695520","subitem_source_identifier_type":"NCID"}]},"item_10001_version_type_20":{"attribute_name":"出版タイプ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_1715043197608":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open 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islets","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"rat glucagon promoter (RGP)","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"adoptive transfer","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"CD4+ and CD8+ T cells","subitem_subject_language":"en","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":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by Transgenic Paracrine TGF-β1","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Abrogation of Autoimmune Diabetes in Nonobese Diabetic Mice and Protection against Effector Lymphocytes by 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