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dc.contributor.authorSzabo, Gyongyi
dc.contributor.authorDolganiuc, Angela
dc.date2022-08-11T08:08:37.000
dc.date.accessioned2022-08-23T16:01:33Z
dc.date.available2022-08-23T16:01:33Z
dc.date.issued2008-02-27
dc.date.submitted2010-04-21
dc.identifier.citationCrit Rev Immunol. 2008;28(1):61-94.
dc.identifier.issn1040-8401 (Linking)
dc.identifier.pmid18298384
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31150
dc.description.abstractViral infections represent a major source of acute and chronic human disease. The immune system plays a central role in the elimination of viruses through its ability to recognize pathogens and to induce virus-specific cellular activation, accompanied by a robust production of soluble molecules with antiviral effects. Interferons are among the most powerful natural soluble antiviral molecules. Upon viral infection, interferons are produced by a variety of cell types, with immune cells being the main contributors. The immune system works as a well-orchestrated team composed of multiple cell types. The mechanisms of intercellular cooperation that includes dendritic cells (DCs), their soluble factors, and different types of immune cells are yet to be fully understood. Further, the effects of viral infections on interimmune cooperation need to be investigated. In this review, we define the role of plasmacytoid dendritic cells (PDC) and PDC-derived interferon alpha (IFNalpha) during viral infections. Specifically, we address the mechanisms of IFNalpha induction and the cooperation between PDC, PDC-derived IFNalpha and T cells, B cells, NK, iNKT, and myeloid dendric cells in antiviral immune responses.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18298384&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.begellhouse.com/journals/2ff21abf44b19838,2edb2d8b0ae484ee,16587c0d64a8a11c.html
dc.subjectAnimals
dc.subjectAntiviral Agents
dc.subjectB-Lymphocytes
dc.subjectDNA Virus Infections
dc.subjectDendritic Cells
dc.subjectHumans
dc.subjectImmunologic Factors
dc.subjectInterferon-alpha
dc.subjectIntracellular Signaling Peptides and Proteins
dc.subjectKiller Cells, Natural
dc.subjectLymphocyte Activation
dc.subjectRNA Virus Infections
dc.subjectT-Lymphocyte Subsets
dc.subjectToll-Like Receptors
dc.subjectViruses
dc.subjectGastroenterology
dc.subjectImmunology and Infectious Disease
dc.titleThe role of plasmacytoid dendritic cell-derived IFN alpha in antiviral immunity
dc.typeJournal Article
dc.source.journaltitleCritical reviews in immunology
dc.source.volume28
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gastroenterology_pp/74
dc.identifier.contextkey1282373
html.description.abstract<p>Viral infections represent a major source of acute and chronic human disease. The immune system plays a central role in the elimination of viruses through its ability to recognize pathogens and to induce virus-specific cellular activation, accompanied by a robust production of soluble molecules with antiviral effects. Interferons are among the most powerful natural soluble antiviral molecules. Upon viral infection, interferons are produced by a variety of cell types, with immune cells being the main contributors. The immune system works as a well-orchestrated team composed of multiple cell types. The mechanisms of intercellular cooperation that includes dendritic cells (DCs), their soluble factors, and different types of immune cells are yet to be fully understood. Further, the effects of viral infections on interimmune cooperation need to be investigated. In this review, we define the role of plasmacytoid dendritic cells (PDC) and PDC-derived interferon alpha (IFNalpha) during viral infections. Specifically, we address the mechanisms of IFNalpha induction and the cooperation between PDC, PDC-derived IFNalpha and T cells, B cells, NK, iNKT, and myeloid dendric cells in antiviral immune responses.</p>
dc.identifier.submissionpathgastroenterology_pp/74
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.source.pages61-94


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