{"created":"2023-07-27T06:38:45.472414+00:00","id":26938,"links":{},"metadata":{"_buckets":{"deposit":"cc5526a3-c54c-45b2-b598-31a87936518b"},"_deposit":{"created_by":3,"id":"26938","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"26938"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00026938","sets":["1761:1762:1763"]},"author_link":["20219","45571","45569","20218","45570"],"item_4_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2008-10-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"10","bibliographicPageEnd":"3430","bibliographicPageStart":"3420","bibliographicVolumeNumber":"118","bibliographic_titles":[{"bibliographic_title":"Journal of Clinical Investigation"}]}]},"item_4_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"EAE is a mouse T cell-mediated autoimmune disease of the CNS used to model the human condition MS. The contributions of B cells to EAE initiation and progression are unclear. In this study, we have shown that EAE disease initiation and progression are differentially influenced by the depletion of B cells from mice with otherwise intact immune systems. CD20 antibody-mediated B cell depletion before EAE induction substantially exacerbated disease symptoms and increased encephalitogenic T cell influx into the CNS. Increased symptom severity resulted from the depletion of a rare IL-10-producing CD1d hiCD5+ regulatory B cell subset (B10 cells), since the adoptive transfer of splenic B10 cells before EAE induction normalized EAE in B cell-depleted mice. While transfer of regulatory B10 cells was maximally effective during early EAE initiation, they had no obvious role during disease progression. Rather, B cell depletion during EAE disease progression dramatically suppressed symptoms. Specifically, B cells were required for the generation of CD4+ T cells specific for CNS autoantigen and the entry of encephalitogenic T cells into the CNS during disease progression. These results demonstrate reciprocal regulatory roles for B cells during EAE immunopathogenesis. The therapeutic effect of B cell depletion for the treatment of autoimmunity may therefore depend on the relative contributions and the timing of these opposing B cell activities during the course of disease initiation and pathogenesis.","subitem_description_type":"Abstract"}]},"item_4_publisher_17":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"American Society for Clinical Investigation"}]},"item_4_relation_12":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1172/JCI36030","subitem_relation_type_select":"DOI"}}]},"item_4_source_id_11":{"attribute_name":"NCID","attribute_value_mlt":[{"subitem_source_identifier":"AA00695520","subitem_source_identifier_type":"NCID"}]},"item_4_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0021-9738","subitem_source_identifier_type":"ISSN"}]},"item_4_version_type_25":{"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_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Matsushita, Takashi"}],"nameIdentifiers":[{},{},{},{}]},{"creatorNames":[{"creatorName":"Yanaba, Koichi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Bouaziz, Jean-David"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Fujimoto, Manabu"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"Tedder, Thomas F."}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-10-05"}],"displaytype":"detail","filename":"ME-PR-MATSUSHITA-T-3420.pdf","filesize":[{"value":"719.4 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"ME-PR-MATSUSHITA-T-3420.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/26938/files/ME-PR-MATSUSHITA-T-3420.pdf"},"version_id":"51a873d8-390a-49df-84ff-01abceb397ce"}]},"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":"Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression"}]},"item_type_id":"4","owner":"3","path":["1763"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-10-05"},"publish_date":"2017-10-05","publish_status":"0","recid":"26938","relation_version_is_last":true,"title":["Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-07-27T21:16:04.418116+00:00"}