{"created":"2023-05-15T15:16:58.263749+00:00","id":2965,"links":{},"metadata":{"_buckets":{"deposit":"08eb9613-419c-4d24-bf9e-7eb7bf849cc9"},"_deposit":{"created_by":12,"id":"2965","owners":[12],"pid":{"revision_id":0,"type":"depid","value":"2965"},"status":"published"},"_oai":{"id":"oai:obihiro.repo.nii.ac.jp:00002965","sets":["242:243"]},"author_link":["48","221","210","140","258","145"],"item_6_alternative_title_1":{"attribute_name":"その他（別言語等）の研究課題名","attribute_value_mlt":[{"subitem_alternative_title":"Immunopotentiatroy Effects of TLA and Obioactin on the Acquired Immunodeficiency Syndroms (AIDS) in 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篤志","lang":"ja"}],"familyNames":[{"familyName":"Saito","familyNameLang":"en"},{"familyName":"齋藤","familyNameLang":"ja"}],"givenNames":[{"givenName":"Atsushi","givenNameLang":"en"},{"givenName":"篤志","givenNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"210","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"9000004409900","nameIdentifierScheme":"CiNii 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弘之","lang":"ja"}],"familyNames":[{"familyName":"Miura","familyNameLang":"en"},{"familyName":"三浦","familyNameLang":"ja"}],"givenNames":[{"givenName":"Hiroyuki","givenNameLang":"en"},{"givenName":"弘之","givenNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"145","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"90003079","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=90003079"}]},{"contributorAffiliations":[{"contributorAffiliationNameIdentifiers":[{"contributorAffiliationNameIdentifier":"","contributorAffiliationScheme":"ISNI","contributorAffiliationURI":"http://www.isni.org/isni/"}],"contributorAffiliationNames":[{"contributorAffiliationName":"","contributorAffiliationNameLang":"ja"}]}],"contributorNames":[{"contributorName":"Hirose, Tsuneo","lang":"en"},{"contributorName":"広瀬, 恒夫","lang":"ja"}],"familyNames":[{"familyName":"Hirose","familyNameLang":"en"},{"familyName":"広瀬","familyNameLang":"ja"}],"givenNames":[{"givenName":"Tsuneo","givenNameLang":"en"},{"givenName":"恒夫","givenNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"48","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"9000001174955","nameIdentifierScheme":"CiNii ID","nameIdentifierURI":"http://ci.nii.ac.jp/nrid/9000001174955"},{"nameIdentifier":"60003076","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=60003076"}]}]},"item_6_description_10":{"attribute_name":"研究代表者番号","attribute_value_mlt":[{"subitem_description":"10003071","subitem_description_type":"Other"}]},"item_6_description_11":{"attribute_name":"研究機関","attribute_value_mlt":[{"subitem_description":"帯広畜産大学","subitem_description_type":"Other"}]},"item_6_description_13":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"トキソプラズマ原虫の可溶性抗原成分(TLA)は生物応答修飾物質(BRM)の1つとして宿主生体に非特異的感染防御能を極めて強く賦与し、現象的には生体内でのTーリンパ球増殖とガンマ-インタ-フェロンなどのサイトカインを産生することが明らかになっている。一方、サイトカイン中マクロファ-ジ活性化因子の生物学的解析からマクロファ-ジ内トキソプラズマ原虫の増殖を強く抑制する作用物質(オビオアクチン)を検出し、免疫調整作用のあることを見付けている。そこで、これらの免疫調整・賦活物質のウイルス感染に伴うトキンブラズマ感染症および腫瘍増殖に対する影響について検討を加えた。免疫賦活物質としてのTLAをマウスに投与するとナチュラル・キラ-(NK)細胞、Tーリンパ球およびBーリンパ球が脾臓および肝内に増加する。健康マウスにトキソプラズマ原虫を感染すると、感染初期にNK細胞及びTー細胞が脾臓内に著増するが、強毒株トキソプラズマ原虫増殖によってマウスは全例死亡する。一方、TLA前感作したマウスに同一強毒株トキソプラズマを感染しても30〜40%耐過生残する。その生残例の脾臓及び肝臓内にNK細胞とTー細胞の集蔟が極めて顕著であり、大型円形細胞の浸じゅんが多数認められた。そこでTLAで感作あるいは非感作マウスの脾臓内単核細胞を、TLAと共にIn Vitroで1日〜6日間連続培養し、その培養細胞をEffector細胞として、NK細胞非感受性細胞(P,815)とNK感受性細胞(YACー1)のTarget細胞に対する細胞障害性試験をおこなった。その結果、培養3〜6日目に強い細胞障害活性が発現し、大型のリンホカイン活性キラ-細胞(LAK)およびNK様LAK細胞がTLAによって誘導されることが明らかになった。そして、未公表デ-タ-ではあるが、このキラ-細胞誘導にはマクロ-ファ-ジの在存が必須であり、そのマクロファ-ジはキラ-細胞誘導細胞との接着が重要な条件である可能性が推察された。","subitem_description_language":"ja","subitem_description_type":"Abstract"},{"subitem_description":"Toxoplasma gondii has been reported to stimulate non-specific resistance to rodent malaria and babesia diseases. Mice that were treated systemically with Toxoplasma lysate antigen (TLA) were highly resistant to infection with Plasmodium berghei and Babesia rodhaini. Consequently, studies of the behavior of lymphocytes and natural killer (NK) cells and lymphokines activated killer (LAK) cells from TLA sensitized animals may clarify the factors responsible for resistance to infection with protozoan parasites and with tumors.\nWhen adult BALB/C mice were sensitized with two intramuscular injection of TLA at 2 week interval, the numbers of Sig(+), Thy-1(+), Lyt-2, 2(+), and asialo GM1(+) cells in the spleen, liver and peripheral blood increased by 2 to 4 times over those found in unsensitized mice of the same age. When TLA-sensitized and unsensitized mice were inoculated with Babesia, 4 of 10(40%) of the TLA-sensitized mice survived infection, while none of the unsensitized control mice lived longer than 14 days after infection. By contrast sensitization of nude mice with TLA has no effect on survival, and mice did not live more than 12 days. The number of thymic Thy-1, 2(+) cells decreased in TLA-sensitized and unsensitized BALA/c mice by almost 80% within 10 days after infection. During the same time, the numbers of B cells, T cells, and NK cells increased in the spleen, liver and peripheral blood of both sensitized and unsensitized mice. Especially notable were increases in the numbers of Lyt-2,2 cells in the spleen and blood and increases in numbers of NK cells in the spleen, liver and blood in both TLA-sensitized and unsensitized mice. When spleen cells from TLA-sensitized and unsensitized mice were cultured in the presence or absence of TLA for 6 days, assays for cytotoxicity using NK-insensitive P-815 target cells and NK-sensitive YAC-1 target cells demonstrated higher rates of cytotoxicity in cultures of TLA-sensitized spleen cells. The present results showed clearly that addition of TLA to cultures of TLA-sensitized spleen cells stimulates production of killer cells, such as lymphokine activated killer (LAK) cells and NK-like LAK and/or NK cells. Consequently, resistance of TLA sensitized mice to protozoan infection may be mediated not only by increases in the numbers of Thy-1, 2(+) and asialo GM1(+) cells, but also by quantitative and qualitative variations in these cell types.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_6_description_14":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"平成2年度科学研究費補助金(一般研究A)研究成果報告書","subitem_description_language":"ja","subitem_description_type":"Other"}]},"item_6_description_19":{"attribute_name":"フォーマット","attribute_value_mlt":[{"subitem_description":"application/pdf","subitem_description_type":"Other"}]},"item_6_description_9":{"attribute_name":"研究課題番号","attribute_value_mlt":[{"subitem_description":"62440020","subitem_description_type":"Other"}]},"item_6_text_12":{"attribute_name":"助成元","attribute_value_mlt":[{"subitem_text_language":"ja","subitem_text_value":"科学研究費助成事業"}]},"item_6_version_type_20":{"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_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-01-30"}],"displaytype":"detail","filename":"H3suzuki.pdf","filesize":[{"value":"27.7 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"H3suzuki.pdf","url":"https://obihiro.repo.nii.ac.jp/record/2965/files/H3suzuki.pdf"},"version_id":"d9b5c661-45d1-4e2f-a34e-f529b806251b"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_researcher":{"attribute_name":"研究代表者","attribute_type":"creator","attribute_value_mlt":[{"creatorAffiliations":[{"affiliationNameIdentifiers":[{"affiliationNameIdentifier":"","affiliationNameIdentifierScheme":"ISNI","affiliationNameIdentifierURI":"http://www.isni.org/isni/"}],"affiliationNames":[{"affiliationName":"","affiliationNameLang":"ja"}]}],"creatorNames":[{"creatorName":"Suzuki, Naoyoshi","creatorNameLang":"en"},{"creatorName":"鈴木, 直義","creatorNameLang":"ja"}],"familyNames":[{"familyName":"Suzuki","familyNameLang":"en"},{"familyName":"鈴木","familyNameLang":"ja"}],"givenNames":[{"givenName":"Naoyoshi","givenNameLang":"en"},{"givenName":"直義","givenNameLang":"ja"}],"nameIdentifiers":[{"nameIdentifier":"258","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"9000005634551","nameIdentifierScheme":"CiNii ID","nameIdentifierURI":"http://ci.nii.ac.jp/nrid/9000005634551"},{"nameIdentifier":"10003071","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=10003071"}]}]},"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":"後天性免疫不全症(AIDS)の治療におけるトキソプラズマ抗原の役割に関する研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"後天性免疫不全症(AIDS)の治療におけるトキソプラズマ抗原の役割に関する研究","subitem_title_language":"ja"}]},"item_type_id":"6","owner":"12","path":["243"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2008-01-09"},"publish_date":"2008-01-09","publish_status":"0","recid":"2965","relation_version_is_last":true,"title":["後天性免疫不全症(AIDS)の治療におけるトキソプラズマ抗原の役割に関する研究"],"weko_creator_id":"12","weko_shared_id":-1},"updated":"2024-07-02T03:23:58.919596+00:00"}