{"created":"2023-07-27T07:00:28.279996+00:00","id":60413,"links":{},"metadata":{"_buckets":{"deposit":"66941e6f-c60b-451b-9acf-170ac9fd1970"},"_deposit":{"created_by":18,"id":"60413","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"60413"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00060413","sets":["2812:2813:2839"]},"author_link":["20433","22228"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"1996-04-14","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"3p.","bibliographicVolumeNumber":"1993 – 1994","bibliographic_titles":[{"bibliographic_title":"平成6(1994)年度 科学研究費補助金 一般研究(B) 研究成果報告書概要"},{"bibliographic_title":"1994 Fiscal Year Final Research Report Summary","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":"本研究では,EBV初感染伝染性単核症(IM)を一つのモデルとして活性化に伴うT細胞の生理的細胞死の背景を検討,以下の成績が得られた.\n1)IM活性化T細胞は,健康者メモリーT細胞とCD45RO抗原やアポトーシス媒介性細胞表面分子のFas抗原発現は大差ないが,健康者メモリーT細胞と異なりIM活性化T細胞は試験官内で容易に著明なアポトーシスが起こす.T細胞のアポトーシス誘導には細胞の内的条件が重要と考えられ,T細胞のアポトーシスに関わる新たな細胞膜分子を同定する意味で,IM患者リンパ球を免疫原に単クローン抗体IMN3.1抗体を得た.\n2)アポトーシス抑制遺伝子産物のBcl-2は,健康者メモリーT細胞で強く発現するが,IM活性化T細胞では欠如する.Bcl-2発現の欠損ないし減弱は,顆粒球や単球のような半減期の短い白血球でも観察される.顆粒球や単球ではFas抗原の構成的発現がみられ,Bcl-2微弱発現に対応して顆粒球や単球が抗Fas抗体によりアポトーシスが促進された.これらの結果は,Bcl-2発現の強弱がFas/リガンドに対する細胞の感受性に一部関係すること,Fas/リガンド系が免疫反応のみならず炎症に関わる血液系細胞をも標的として作用すること示した.\n3)癌遺伝子産物のp53は細胞のアポトーシス誘導を促進する作用があり,点突然変異により生じた変異p53はその作用がなく,癌細胞の生成や不死化を導く.伝染性単核症活性化T細胞ではp53発現はないが,正常者リンパ球を放射線照射によりアポトーシス死を誘導した場合にp53発現が誘導される.放射線照射性アポトーシスに付随したp53発現が,CD4^+T細胞,CD8^+T細胞やB細胞でみられるのに反して,NK細胞やγδ型のT細胞抗原受容体をもつT細胞ではp53発現を伴わないことを示し,リンパ球のアポトーシス誘導に関わる細胞内条件としてのp53の役割には多様性のあることを明かにした.","subitem_description_type":"Abstract"},{"subitem_description":"We employed EBV-induced infectious mononucleosis (IM) as a model of activated T cell death to elucidate cellular requirements for induction of T cell death by activation with viral infection. Obtained results are as follows :\n1)Both activated T cells in acute IM patients and memory T cells in normal persons express CD45RO and Fas antigen, which can mediate apoptosis. Unlike memory T cells, activated T cells in IM easily undergo apoptotic cell death after on a simple incubation in vitro. By immunizing mice with IM cells, we obtained a novel mouse monoclonal antibody, termed IMN3.1, which was marked to react with apoptosis-prone T cells. Molecular cloning of IMN3.1-identified antigen is in progress.\n2)Seemingly supporting their susceptibility to apoptosis, activated T cells in IM lacked expression of Bcl-2, which have a preventive function against apoptotic cell death. Low or absent expression of Bcl-2 was observed on granulocytes and monocytes, both of which have shorter life-spans. The important finding was that anti-Fas antibody could accelerated apoptotic cell death in granulocytes and monocytes. These observations suggest that the Fas antigen/ligand system may play a key role in resolution of inflammatory and immune responses.\n3)The mutation of the p53 oncogene is thought to lead to oncogenosis in human malignancies. Expression of p53 was not found in activated T cells in IM patients, although they were sucseptible to apoptosis. Ionizing irradiation could induce p53 expression on the whole population of peripheral blood lymphocytes, concomitant with marked apoptosis. However, we found a marked difference of lymphocyte subpopulations regarding p53 induction. Induction of p53 in CD4^+ T,CD8^+ T and B cells after irradiation was prominent. In contrast, neither TCR-gamma/delta^+ T cells nor NK cells showed identifiable levels of p53. The results suggest that radiation-induced lymphocytic apoptosis may be mediated by p53-dependent or-independent mechanisms.","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:05454284, 研究期間(年度):1993 – 1994","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「EBV感染におけるT細胞の活性化と細胞死のメカニズムに関する研究」課題番号05454284\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（https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-05454284/054542841994kenkyu_seika_hokoku_gaiyo/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学医学部・附属病院","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00066661","subitem_identifier_reg_type":"JaLC"}]},"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=10143885"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=10143885","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-05454284/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-05454284/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-05454284/054542841994kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-05454284/054542841994kenkyu_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":"2022-06-30"}],"displaytype":"detail","filename":"HO-PR-MIYAWAKI-T-kaken 1996-3p.pdf","filesize":[{"value":"101.3 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"HO-PR-MIYAWAKI-T-kaken 1996-3p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/60413/files/HO-PR-MIYAWAKI-T-kaken 1996-3p.pdf"},"version_id":"23408e57-c96f-4636-a638-bb97d666f5f7"}]},"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":"EBV感染におけるT細胞の活性化と細胞死のメカニズムに関する研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"EBV感染におけるT細胞の活性化と細胞死のメカニズムに関する研究"},{"subitem_title":"A Study on cellular requirements for apoptotic cell death of activated T cells in EBV infection","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2839"],"pubdate":{"attribute_name":"公開日","attribute_value":"2022-06-30"},"publish_date":"2022-06-30","publish_status":"0","recid":"60413","relation_version_is_last":true,"title":["EBV感染におけるT細胞の活性化と細胞死のメカニズムに関する研究"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T12:43:59.289110+00:00"}