{"@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/1363670320326983552.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1128/jvi.79.9.5507-5515.2005"}},{"identifier":{"@type":"URI","@value":"https://journals.asm.org/doi/pdf/10.1128/JVI.79.9.5507-5515.2005"}}],"dc:title":[{"@value":"Inhibition of Toll-Like Receptor 7- and 9-Mediated Alpha/Beta Interferon Production in Human Plasmacytoid Dendritic Cells by Respiratory Syncytial Virus and Measles Virus"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>ABSTRACT</jats:title>\n          <jats:p>\n            Human plasmacytoid dendritic cells (PDC) are key sentinels alerting both innate and adaptive immune responses through production of huge amounts of alpha/beta interferon (IFN). IFN induction in PDC is triggered by outside-in signal transduction pathways through Toll-like receptor 7 (TLR7) and TLR9 as well as by recognition of cytosolic virus-specific patterns. TLR7 and TLR9 ligands include single-stranded RNA and CpG-rich DNA, respectively, as well as synthetic derivatives thereof which are being evaluated as therapeutic immune modulators promoting Th1 immune responses. Here, we identify the first viruses able to block IFN production by PDC. Both TLR-dependent and -independent IFN responses are abolished in human PDC infected with clinical isolates of respiratory syncytial virus (RSV), RSV strain A2, and measles virus Schwarz, in contrast to RSV strain Long, which we previously identified as a potent IFN inducer in human PDC (Hornung et al., J. Immunol.\n            <jats:bold>173:</jats:bold>\n            5935-5943, 2004). Notably, IFN synthesis of PDC activated by the TLR7 and TLR9 agonists resiquimod (R848) and CpG oligodeoxynucleotide 2216 is switched off by subsequent infection by RSV A2 and measles virus. The capacity of RSV and measles virus of human PDC to shut down IFN production should contribute to the characteristic features of these viruses, such as Th2-biased immune pathology, immune suppression, and superinfection.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1383670320326983555","@type":"Researcher","foaf:name":[{"@value":"Jörg Schlender"}],"jpcoar:affiliationName":[{"@value":"Max von Pettenkofer Institute and Gene Center"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983554","@type":"Researcher","foaf:name":[{"@value":"Veit Hornung"}],"jpcoar:affiliationName":[{"@value":"Division of Clinical Pharmacology, Department of Internal Medicine, Ludwig-Maximilians-Universität München, Munich, Germany"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983561","@type":"Researcher","foaf:name":[{"@value":"Stefan Finke"}],"jpcoar:affiliationName":[{"@value":"Max von Pettenkofer Institute and Gene Center"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983556","@type":"Researcher","foaf:name":[{"@value":"Margit Günthner-Biller"}],"jpcoar:affiliationName":[{"@value":"Division of Clinical Pharmacology, Department of Internal Medicine, Ludwig-Maximilians-Universität München, Munich, Germany"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983559","@type":"Researcher","foaf:name":[{"@value":"Sabrina Marozin"}],"jpcoar:affiliationName":[{"@value":"Max von Pettenkofer Institute and Gene Center"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983557","@type":"Researcher","foaf:name":[{"@value":"Krzysztof Brzózka"}],"jpcoar:affiliationName":[{"@value":"Max von Pettenkofer Institute and Gene Center"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983553","@type":"Researcher","foaf:name":[{"@value":"Sharareh Moghim"}],"jpcoar:affiliationName":[{"@value":"Max von Pettenkofer Institute and Gene Center"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983558","@type":"Researcher","foaf:name":[{"@value":"Stefan Endres"}],"jpcoar:affiliationName":[{"@value":"Division of Clinical Pharmacology, Department of Internal Medicine, Ludwig-Maximilians-Universität München, Munich, Germany"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983560","@type":"Researcher","foaf:name":[{"@value":"Gunther Hartmann"}],"jpcoar:affiliationName":[{"@value":"Division of Clinical Pharmacology, Department of Internal Medicine, Ludwig-Maximilians-Universität München, Munich, Germany"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670320326983552","@type":"Researcher","foaf:name":[{"@value":"Karl-Klaus Conzelmann"}],"jpcoar:affiliationName":[{"@value":"Max von Pettenkofer Institute and Gene Center"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"0022538X"},{"@type":"EISSN","@value":"10985514"}],"prism:publicationName":[{"@value":"Journal of Virology"}],"dc:publisher":[{"@value":"American Society for Microbiology"}],"prism:publicationDate":"2005-05","prism:volume":"79","prism:number":"9","prism:startingPage":"5507","prism:endingPage":"5515"},"reviewed":"false","dc:rights":["https://journals.asm.org/non-commercial-tdm-license"],"url":[{"@id":"https://journals.asm.org/doi/pdf/10.1128/JVI.79.9.5507-5515.2005"}],"createdAt":"2005-04-12","modifiedAt":"2022-03-05","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050869456409419136","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Dendritic cell subsets involved in type I IFN induction in mouse measles virus infection models"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002217484375552","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Recognition of Viral RNA by Pattern Recognition Receptors in the Induction of Innate Immunity and Excessive Inflammation During Respiratory Viral Infections"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002220912191488","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Plasmacytoid Dendritic Cells Promote Host Defense against Acute Pneumovirus Infection via the TLR7–MyD88-Dependent Signaling Pathway"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285710962472576","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Human Metapneumovirus M2-2 Protein Acts as a Negative Regulator of Alpha Interferon Production by Plasmacytoid Dendritic Cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285710964193536","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"A Tryptophan-Rich Motif in the Human Parainfluenza Virus Type 2 V Protein Is Critical for the Blockade of Toll-Like Receptor 7 (TLR7)- and TLR9-Dependent Signaling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285710965319040","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Human Parainfluenza Virus Type 2 V Protein Inhibits TRAF6-Mediated Ubiquitination of IRF7 To Prevent TLR7- and TLR9-Dependent Interferon Induction"}]},{"@id":"https://cir.nii.ac.jp/crid/1360565168420959744","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Measles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleukin-1β Secretion"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205736309760","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Poly(U) and CpG ameliorate the unbalanced T cell immunity and pneumonia of mice with RSV vaccine-enhanced 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