Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity▿
Identifieur interne : 002446 ( Pmc/Checkpoint ); précédent : 002445; suivant : 002447Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity▿
Auteurs : Erin L. Lousberg ; Cara K. Fraser ; Michael G. Tovey ; Kerrilyn R. Diener ; John D. HayballSource :
- Journal of Virology [ 0022-538X ] ; 2010.
Abstract
Type I interferons (IFNs) are considered to be important mediators of innate immunity due to their inherent antiviral activity, ability to drive the transcription of a number of genes involved in viral clearance, and their role in the initiation of innate and adaptive immune responses. Due to the central role of type I IFNs, we sought to determine their importance in the generation of immunity to a recombinant vaccine vector fowlpox virus (FPV). In analyzing the role of type I IFNs in immunity to FPV, we show that they are critical to the secretion of a number of innate and proinflammatory cytokines, including type I IFNs themselves as well as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-α), IL-6, and IL-1β, and that deficiency leads to enhanced virus-mediated antigen expression. Interestingly, however, type I IFNs were not required for adaptive immune responses to recombinant FPV even though plasmacytoid dendritic cells (pDCs), the primary producers of type I IFNs, have been shown to be requisite for this to occur. Furthermore, we provide evidence that the importance of pDCs may lie in their ability to capture and present virally derived antigen to T cells rather than in their capacity as professional type I IFN-producing cells.
Url:
DOI: 10.1128/JVI.02618-09
PubMed: 20410285
PubMed Central: 2903286
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity<xref ref-type="fn" rid="fn2">▿</xref> </title><author><name sortKey="Lousberg, Erin L" sort="Lousberg, Erin L" uniqKey="Lousberg E" first="Erin L." last="Lousberg">Erin L. Lousberg</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Fraser, Cara K" sort="Fraser, Cara K" uniqKey="Fraser C" first="Cara K." last="Fraser">Cara K. Fraser</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Tovey, Michael G" sort="Tovey, Michael G" uniqKey="Tovey M" first="Michael G." last="Tovey">Michael G. Tovey</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Diener, Kerrilyn R" sort="Diener, Kerrilyn R" uniqKey="Diener K" first="Kerrilyn R." last="Diener">Kerrilyn R. Diener</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hayball, John D" sort="Hayball, John D" uniqKey="Hayball J" first="John D." last="Hayball">John D. 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Lousberg</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Fraser, Cara K" sort="Fraser, Cara K" uniqKey="Fraser C" first="Cara K." last="Fraser">Cara K. Fraser</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Tovey, Michael G" sort="Tovey, Michael G" uniqKey="Tovey M" first="Michael G." last="Tovey">Michael G. Tovey</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Diener, Kerrilyn R" sort="Diener, Kerrilyn R" uniqKey="Diener K" first="Kerrilyn R." last="Diener">Kerrilyn R. Diener</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Hayball, John D" sort="Hayball, John D" uniqKey="Hayball J" first="John D." last="Hayball">John D. Hayball</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Type I interferons (IFNs) are considered to be important mediators of innate immunity due to their inherent antiviral activity, ability to drive the transcription of a number of genes involved in viral clearance, and their role in the initiation of innate and adaptive immune responses. Due to the central role of type I IFNs, we sought to determine their importance in the generation of immunity to a recombinant vaccine vector fowlpox virus (FPV). In analyzing the role of type I IFNs in immunity to FPV, we show that they are critical to the secretion of a number of innate and proinflammatory cytokines, including type I IFNs themselves as well as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-α), IL-6, and IL-1β, and that deficiency leads to enhanced virus-mediated antigen expression. Interestingly, however, type I IFNs were not required for adaptive immune responses to recombinant FPV even though plasmacytoid dendritic cells (pDCs), the primary producers of type I IFNs, have been shown to be requisite for this to occur. Furthermore, we provide evidence that the importance of pDCs may lie in their ability to capture and present virally derived antigen to T cells rather than in their capacity as professional type I IFN-producing cells.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id><journal-id journal-id-type="publisher-id">jvirol</journal-id><journal-title-group><journal-title>Journal of Virology</journal-title></journal-title-group><issn pub-type="ppub">0022-538X</issn><issn pub-type="epub">1098-5514</issn><publisher><publisher-name>American Society for Microbiology (ASM)</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">20410285</article-id><article-id pub-id-type="pmc">2903286</article-id><article-id pub-id-type="publisher-id">2618-09</article-id><article-id pub-id-type="doi">10.1128/JVI.02618-09</article-id><article-categories><subj-group subj-group-type="heading"><subject>Virus-Cell Interactions</subject></subj-group></article-categories><title-group><article-title>Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity<xref ref-type="fn" rid="fn2">▿</xref> </article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lousberg</surname><given-names>Erin L.</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff1">4</xref></contrib><contrib contrib-type="author"><name><surname>Fraser</surname><given-names>Cara K.</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff1">4</xref></contrib><contrib contrib-type="author"><name><surname>Tovey</surname><given-names>Michael G.</given-names></name><xref ref-type="aff" rid="aff1">2</xref></contrib><contrib contrib-type="author"><name><surname>Diener</surname><given-names>Kerrilyn R.</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="fn" rid="fn1">†</xref></contrib><contrib contrib-type="author"><name><surname>Hayball</surname><given-names>John D.</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff1">3</xref><xref ref-type="aff" rid="aff1">4</xref><xref ref-type="fn" rid="fn1">†</xref><xref ref-type="corresp" rid="cor1">*</xref></contrib></contrib-group><aff id="aff1">Hanson Institute, SA Pathology, Adelaide, South Australia, Australia,<label>1</label> Laboratory of Viral Oncology, Institute Andre Lwoff, Villejuif, France,<label>2</label> School of Medicine, University of Adelaide, Adelaide, South Australia, Australia,<label>3</label> Sansom Institute, School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia, Australia<label>4</label></aff><author-notes><corresp id="cor1"><label>*</label>Corresponding author. Mailing address: Sansom Institute, School of Pharmacy and Medical Science, University of South Australia, North Tce., Adelaide, South Australia, Australia 5000. Phone: 61 8 8302 1202. Fax: 61 8 8302 2389. E-mail: <email>john.hayball@unisa.edu.au</email></corresp><fn id="fn1"><label>†</label><p>K.R.D. and J.D.H. contributed equally to this work.</p></fn></author-notes><pub-date pub-type="ppub"><month>7</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>21</day><month>4</month><year>2010</year></pub-date><volume>84</volume><issue>13</issue><fpage>6549</fpage><lpage>6563</lpage><history><date date-type="received"><day>14</day><month>12</month><year>2009</year></date><date date-type="accepted"><day>9</day><month>4</month><year>2010</year></date></history><permissions><copyright-statement>Copyright © 2010, American Society for Microbiology</copyright-statement><copyright-year>2010</copyright-year></permissions><self-uri xlink:title="pdf" xlink:href="zjv01310006549.pdf"></self-uri><abstract><p>Type I interferons (IFNs) are considered to be important mediators of innate immunity due to their inherent antiviral activity, ability to drive the transcription of a number of genes involved in viral clearance, and their role in the initiation of innate and adaptive immune responses. Due to the central role of type I IFNs, we sought to determine their importance in the generation of immunity to a recombinant vaccine vector fowlpox virus (FPV). In analyzing the role of type I IFNs in immunity to FPV, we show that they are critical to the secretion of a number of innate and proinflammatory cytokines, including type I IFNs themselves as well as interleukin-12 (IL-12), tumor necrosis factor-alpha (TNF-α), IL-6, and IL-1β, and that deficiency leads to enhanced virus-mediated antigen expression. Interestingly, however, type I IFNs were not required for adaptive immune responses to recombinant FPV even though plasmacytoid dendritic cells (pDCs), the primary producers of type I IFNs, have been shown to be requisite for this to occur. Furthermore, we provide evidence that the importance of pDCs may lie in their ability to capture and present virally derived antigen to T cells rather than in their capacity as professional type I IFN-producing cells.</p></abstract></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Diener, Kerrilyn R" sort="Diener, Kerrilyn R" uniqKey="Diener K" first="Kerrilyn R." last="Diener">Kerrilyn R. Diener</name><name sortKey="Fraser, Cara K" sort="Fraser, Cara K" uniqKey="Fraser C" first="Cara K." last="Fraser">Cara K. Fraser</name><name sortKey="Hayball, John D" sort="Hayball, John D" uniqKey="Hayball J" first="John D." last="Hayball">John D. Hayball</name><name sortKey="Lousberg, Erin L" sort="Lousberg, Erin L" uniqKey="Lousberg E" first="Erin L." last="Lousberg">Erin L. Lousberg</name><name sortKey="Tovey, Michael G" sort="Tovey, Michael G" uniqKey="Tovey M" first="Michael G." last="Tovey">Michael G. 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