{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360002218179078528.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/j.1349-7006.2009.01296.x"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1349-7006.2009.01296.x"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1349-7006.2009.01296.x"}},{"identifier":{"@type":"PMID","@value":"19694752"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Delayed growth of EL4 lymphoma in SR‐A‐deficient mice is due to upregulation of nitric oxide and interferon‐γ production by tumor‐associated macrophages"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>Class A scavenger receptors (SR‐A, CD204) are highly expressed in tumor‐associated macrophages (TAM). To investigate the function of SR‐A in TAM, wild‐type and SR‐A‐deficient (SR‐A<jats:sup>−/−</jats:sup>) mice were injected with EL4 cells. Although these groups of mice did not differ in the numbers of infiltrating macrophages and lymphocytes and in neovascularization, SR‐A<jats:sup>−/−</jats:sup> mice had delayed growth of EL4 tumors. Expression of inducible nitric oxide (NO) synthase and interferon (IFN)‐γ mRNA increased significantly in tumor tissues from SR‐A<jats:sup>−/−</jats:sup> mice. Engulfment of necrotic EL4 cells induced upregulation of NO and IFN‐γ production by cultured macrophages, and production of NO and IFN‐γ increased in SR‐A<jats:sup>−/−</jats:sup> macrophages <jats:italic>in vitro</jats:italic>. IFN‐β production by cultured macrophages was also elevated in SR‐A<jats:sup>−/−</jats:sup> macrophages <jats:italic>in vitro</jats:italic>. These results suggested that the antitumor activity of macrophages increased in SR‐A<jats:sup>−/−</jats:sup> mice because of upregulation of NO and IFN‐γ production. These data indicate an important role of SR‐A in regulating TAM function by inhibiting toll‐like receptor (TLR)4–IFN‐β signaling. (<jats:italic>Cancer Sci</jats:italic> 2009); 00: 000–000)</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380566396356870020","@type":"Researcher","foaf:name":[{"@value":"Yoshihiro Komohara"}]},{"@id":"https://cir.nii.ac.jp/crid/1380566396356870017","@type":"Researcher","foaf:name":[{"@value":"Kenichi Takemura"}]},{"@id":"https://cir.nii.ac.jp/crid/1380566396356870023","@type":"Researcher","foaf:name":[{"@value":"Xiao Feng Lei"}]},{"@id":"https://cir.nii.ac.jp/crid/1380566396356870019","@type":"Researcher","foaf:name":[{"@value":"Naomi Sakashita"}]},{"@id":"https://cir.nii.ac.jp/crid/1030003658440973057","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"50260716"},{"@type":"NRID","@value":"1000050260716"},{"@type":"NRID","@value":"9000398624393"},{"@type":"NRID","@value":"9000405765363"}],"foaf:name":[{"@value":"Mamoru Harada"}]},{"@id":"https://cir.nii.ac.jp/crid/1380566396356870016","@type":"Researcher","foaf:name":[{"@value":"Hiroshi 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