{"created":"2023-07-27T06:54:58.963669+00:00","id":50591,"links":{},"metadata":{"_buckets":{"deposit":"3d6cbd5f-fbb0-4266-987f-7cb27de73c69"},"_deposit":{"created_by":18,"id":"50591","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"50591"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00050591","sets":["2812:2813:2826"]},"author_link":["91587","1766"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2008-03","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"3p.","bibliographicVolumeNumber":"2006-2007","bibliographic_titles":[{"bibliographic_title":"平成19(2007)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"},{"bibliographic_title":"2007 Fiscal Year Final Research Report","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"1.B細胞の活性化を正に制御する因子であるCD19を欠損したマウスにおいて、DNFB塗布による接触過敏反応を検討した。CD19欠損マウスでは、免疫不全傾向を有し腹腔内B-1細胞が著明に減少しているにもかかわらず、野生型マウスに比べて接触過敏反応が亢進、延長していた。FITC塗布においても同様の結果であった。野生型マウスの脾臓からの辺縁帯B細胞を移入することにより、CD19欠損マウスでの接触過敏反応の亢進は抑制され、辺縁帯B細胞に\"RegulatoryB細胞\"の役割を担う細胞が存在することが示唆された。以上のことから、CD19が接触過敏反応をはじめとするIV型アレルギーの治療のターゲットになりうると考えられた。\n2.自己免疫水疱症の発症機序におけるB細胞の関与を検討するために、患者血清におけるBAFFおよび各種ケモカインの濃度を測定し、発症および重症化に寄与する因子を解析した。BAFFは水疱性類天疱瘡患者において発症直前および発症早期に上昇しており、発症に関与する可能性が考えられたが、尋常性天疱瘡患者においては上昇は認められなかった。一方、ケモカインでは、MCP-1, MIG, IP-10の有意な上昇が水庖性類天庖瘡患者血清で認められた。尋常性天疱瘡患者では各サイトカインともに有意な上昇は認められなかった。このように水庖症のそれぞれの疾患の間で発症機序の相違が考えられた。\n3.全身性エリテマトーデスのモデルであるNZB/NZW F1マウスにおいてもCD19の病態への関与を検討した。CD19を欠損したNZB/NZW F1マウスでは、Regulatory B細胞は欠損しており、これを補充することにより、症状および生存期間の有意な改善が認められ、全身性自己免疫疾患に置いても有望な治療法となりうる可能性が示された。\n4.BAFFを介したB細胞の自己免疫疾患における線維化機序への関与を検討するために、TSKマウスにおいて抗BAFF抗体投与による症状の改善について検討した。抗BAFF抗体によりマウス皮膚の線維化は有意に抑制された。","subitem_description_type":"Abstract"},{"subitem_description":"We assessed the role of the B cell-specific surface molecule CD19 on the development of CHS through examining CD19-deficient mice. CD19 is a member of the Ig superfamily expressed on B cells and follicular dendritic cells, and serves as a positive B-cell response regulator which defines signaling thresholds critical for B cell responses. Contact hypersensitivity (CHS) is a cutaneous immune reaction mediated mainly by Ag-specific effector T cells, and regarded as a model for Th1/Tc1-mediated inflammation, while recent reports have suggested pivotal roles of B cells in CHS. Although CD19-deficient mice are hyposensitive to a variety of transmembrane signals, CD19 loss resulted in increased and prolonged reaction of CHS, suggesting an inhibitory role of CD19 expression in the etiology of CHS. Adoptive transfer experiments revealed that CD19 expression in B cells is recipient mice was required for optimal suppression of CHS response, indicating its role in elicitation phase. Furthermore, spleen B-2 cells, especially marginal zone B cells, from wild type mice were able to normalize exaggerated CHS reactions in CD19-deficient mice. Thus, CD19 expression in B cells is critical for termination of CHS responses, possibly through the function of \"regulatory B cells\". This B cell subset was also capable for improving murine lupus manifestations.\nWe also assessed serum BAFF and chemokine levels in patieits with autoimmune bullous diseases, and examined BAFF roles in TSK mice, an animal model of systemic sclerosis.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:18591239, 研究期間(年度):2006-2007","subitem_description_type":"Other"},{"subitem_description":"出典：「B細胞シグナル伝達を標的とした自己免疫疾患治療法の開発」研究成果報告書　課題番号18591239\n  (KAKEN：科学研究費助成事業データベース（国立情報学研究所）)\n　　　本文データは著者版報告書より作成","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00056900","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学医薬保健研究域医学系"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=90272591"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=90272591","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591239/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591239/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-18591239/185912392007kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-18591239/185912392007kenkyu_seika_hokoku_gaiyo/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-02-21"}],"displaytype":"detail","filename":"ME-PR-FUJIMOTO-M-kaken 2007-3p.pdf","filesize":[{"value":"110.1 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-FUJIMOTO-M-kaken 2007-3p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/50591/files/ME-PR-FUJIMOTO-M-kaken 2007-3p.pdf"},"version_id":"72091cdc-e81d-4796-b70e-f2fb5910a880"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"B細胞シグナル伝達を標的とした自己免疫疾患治療法の開発","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"B細胞シグナル伝達を標的とした自己免疫疾患治療法の開発"},{"subitem_title":"Developmentoftherapies for autoimmune diseases by targeting B cellsignaling","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2826"],"pubdate":{"attribute_name":"公開日","attribute_value":"2020-02-21"},"publish_date":"2020-02-21","publish_status":"0","recid":"50591","relation_version_is_last":true,"title":["B細胞シグナル伝達を標的とした自己免疫疾患治療法の開発"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T14:23:45.233344+00:00"}