Lambda interferon renders epithelial cells of the respiratory and gastrointestinal tracts resistant to viral infections.
Identifieur interne : 001639 ( PubMed/Checkpoint ); précédent : 001638; suivant : 001640Lambda interferon renders epithelial cells of the respiratory and gastrointestinal tracts resistant to viral infections.
Auteurs : Markus Mordstein [Allemagne] ; Eva Neugebauer ; Vanessa Ditt ; Birthe Jessen ; Toni Rieger ; Valeria Falcone ; Frederic Sorgeloos ; Stephan Ehl ; Daniel Mayer ; Georg Kochs ; Martin Schwemmle ; Stephan Günther ; Christian Drosten ; Thomas Michiels ; Peter StaeheliSource :
- Journal of virology [ 1098-5514 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Appareil respiratoire (immunologie), Appareil respiratoire (virologie), Cellules épithéliales (virologie), Cytokines (immunologie), Humains, Immunité innée, Maladies virales (immunologie), Récepteur interféron (déficit), Souris, Souris knockout, Tube digestif (immunologie), Tube digestif (virologie).
- MESH :
- déficit : Récepteur interféron.
- immunologie : Appareil respiratoire, Cytokines, Maladies virales, Tube digestif.
- virologie : Appareil respiratoire, Cellules épithéliales, Tube digestif.
- Animaux, Humains, Immunité innée, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals, Cytokines (immunology), Epithelial Cells (virology), Gastrointestinal Tract (immunology), Gastrointestinal Tract (virology), Humans, Immunity, Innate, Mice, Mice, Knockout, Receptors, Interferon (deficiency), Respiratory System (immunology), Respiratory System (virology), Virus Diseases (immunology).
- MESH :
- chemical , deficiency : Receptors, Interferon.
- chemical , immunology : Cytokines.
- immunology : Gastrointestinal Tract, Respiratory System, Virus Diseases.
- virology : Epithelial Cells, Gastrointestinal Tract, Respiratory System.
- Animals, Humans, Immunity, Innate, Mice, Mice, Knockout.
Abstract
Virus-infected cells secrete a broad range of interferons (IFN) which confer resistance to yet uninfected cells by triggering the synthesis of antiviral factors. The relative contributions of the various IFN subtypes to innate immunity against virus infections remain elusive. IFN-alpha, IFN-beta, and other type I IFN molecules signal through a common, universally expressed cell surface receptor, whereas type III IFN (IFN-lambda) uses a distinct cell-type-specific receptor complex for signaling. Using mice lacking functional receptors for type I IFN, type III IFN, or both, we found that IFN-lambda plays an important role in the defense against several human pathogens that infect the respiratory tract, such as influenza A virus, influenza B virus, respiratory syncytial virus, human metapneumovirus, and severe acute respiratory syndrome (SARS) coronavirus. These viruses were more pathogenic and replicated to higher titers in the lungs of mice lacking both IFN receptors than in mice with single IFN receptor defects. In contrast, Lassa fever virus, which infects via the respiratory tract but primarily replicates in the liver, was not influenced by the IFN-lambda receptor defect. Careful analysis revealed that expression of functional IFN-lambda receptor complexes in the lung and intestinal tract is restricted to epithelial cells and a few other, undefined cell types. Interestingly, we found that SARS coronavirus was present in feces from infected mice lacking receptors for both type I and type III IFN but not in those from mice lacking single receptors, supporting the view that IFN-lambda contributes to the control of viral infections in epithelial cells of both respiratory and gastrointestinal tracts.
DOI: 10.1128/JVI.00272-10
PubMed: 20335250
Affiliations:
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xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Immunité innée</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Virus-infected cells secrete a broad range of interferons (IFN) which confer resistance to yet uninfected cells by triggering the synthesis of antiviral factors. The relative contributions of the various IFN subtypes to innate immunity against virus infections remain elusive. IFN-alpha, IFN-beta, and other type I IFN molecules signal through a common, universally expressed cell surface receptor, whereas type III IFN (IFN-lambda) uses a distinct cell-type-specific receptor complex for signaling. Using mice lacking functional receptors for type I IFN, type III IFN, or both, we found that IFN-lambda plays an important role in the defense against several human pathogens that infect the respiratory tract, such as influenza A virus, influenza B virus, respiratory syncytial virus, human metapneumovirus, and severe acute respiratory syndrome (SARS) coronavirus. These viruses were more pathogenic and replicated to higher titers in the lungs of mice lacking both IFN receptors than in mice with single IFN receptor defects. In contrast, Lassa fever virus, which infects via the respiratory tract but primarily replicates in the liver, was not influenced by the IFN-lambda receptor defect. Careful analysis revealed that expression of functional IFN-lambda receptor complexes in the lung and intestinal tract is restricted to epithelial cells and a few other, undefined cell types. Interestingly, we found that SARS coronavirus was present in feces from infected mice lacking receptors for both type I and type III IFN but not in those from mice lacking single receptors, supporting the view that IFN-lambda contributes to the control of viral infections in epithelial cells of both respiratory and gastrointestinal tracts.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20335250</PMID><DateCompleted><Year>2010</Year><Month>06</Month><Day>08</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>84</Volume><Issue>11</Issue><PubDate><Year>2010</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Lambda interferon renders epithelial cells of the respiratory and gastrointestinal tracts resistant to viral infections.</ArticleTitle><Pagination><MedlinePgn>5670-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00272-10</ELocationID><Abstract><AbstractText>Virus-infected cells secrete a broad range of interferons (IFN) which confer resistance to yet uninfected cells by triggering the synthesis of antiviral factors. The relative contributions of the various IFN subtypes to innate immunity against virus infections remain elusive. IFN-alpha, IFN-beta, and other type I IFN molecules signal through a common, universally expressed cell surface receptor, whereas type III IFN (IFN-lambda) uses a distinct cell-type-specific receptor complex for signaling. Using mice lacking functional receptors for type I IFN, type III IFN, or both, we found that IFN-lambda plays an important role in the defense against several human pathogens that infect the respiratory tract, such as influenza A virus, influenza B virus, respiratory syncytial virus, human metapneumovirus, and severe acute respiratory syndrome (SARS) coronavirus. These viruses were more pathogenic and replicated to higher titers in the lungs of mice lacking both IFN receptors than in mice with single IFN receptor defects. In contrast, Lassa fever virus, which infects via the respiratory tract but primarily replicates in the liver, was not influenced by the IFN-lambda receptor defect. Careful analysis revealed that expression of functional IFN-lambda receptor complexes in the lung and intestinal tract is restricted to epithelial cells and a few other, undefined cell types. Interestingly, we found that SARS coronavirus was present in feces from infected mice lacking receptors for both type I and type III IFN but not in those from mice lacking single receptors, supporting the view that IFN-lambda contributes to the control of viral infections in epithelial cells of both respiratory and gastrointestinal tracts.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mordstein</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Virology, University of Freiburg, Hermann-Herder-Strasse 11, D-79104 Freiburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Neugebauer</LastName><ForeName>Eva</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Ditt</LastName><ForeName>Vanessa</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Jessen</LastName><ForeName>Birthe</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Rieger</LastName><ForeName>Toni</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Falcone</LastName><ForeName>Valeria</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Sorgeloos</LastName><ForeName>Frederic</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Ehl</LastName><ForeName>Stephan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mayer</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Kochs</LastName><ForeName>Georg</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Schwemmle</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Günther</LastName><ForeName>Stephan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Drosten</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Michiels</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Staeheli</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>03</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017471">Receptors, Interferon</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C511668">interferon-lambda protein, mouse</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D041981" MajorTopicYN="N">Gastrointestinal Tract</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017471" MajorTopicYN="N">Receptors, Interferon</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012137" MajorTopicYN="N">Respiratory System</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014777" MajorTopicYN="N">Virus Diseases</DescriptorName><QualifierName UI="Q000276" 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IdType="pubmed">17151098</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Bade-Wurtemberg</li><li>District de Fribourg-en-Brisgau</li></region><settlement><li>Fribourg-en-Brisgau</li></settlement></list><tree><noCountry><name sortKey="Ditt, Vanessa" sort="Ditt, Vanessa" uniqKey="Ditt V" first="Vanessa" last="Ditt">Vanessa Ditt</name><name sortKey="Drosten, Christian" sort="Drosten, Christian" uniqKey="Drosten C" first="Christian" last="Drosten">Christian Drosten</name><name sortKey="Ehl, Stephan" sort="Ehl, Stephan" uniqKey="Ehl S" first="Stephan" last="Ehl">Stephan Ehl</name><name sortKey="Falcone, Valeria" sort="Falcone, Valeria" uniqKey="Falcone V" first="Valeria" last="Falcone">Valeria Falcone</name><name sortKey="Gunther, Stephan" sort="Gunther, Stephan" uniqKey="Gunther S" first="Stephan" last="Günther">Stephan Günther</name><name sortKey="Jessen, Birthe" sort="Jessen, Birthe" uniqKey="Jessen B" first="Birthe" last="Jessen">Birthe Jessen</name><name sortKey="Kochs, Georg" sort="Kochs, Georg" uniqKey="Kochs G" first="Georg" last="Kochs">Georg Kochs</name><name sortKey="Mayer, Daniel" sort="Mayer, Daniel" uniqKey="Mayer D" first="Daniel" last="Mayer">Daniel Mayer</name><name sortKey="Michiels, Thomas" sort="Michiels, Thomas" uniqKey="Michiels T" first="Thomas" last="Michiels">Thomas Michiels</name><name sortKey="Neugebauer, Eva" sort="Neugebauer, Eva" uniqKey="Neugebauer E" first="Eva" last="Neugebauer">Eva Neugebauer</name><name sortKey="Rieger, Toni" sort="Rieger, Toni" uniqKey="Rieger T" first="Toni" last="Rieger">Toni Rieger</name><name sortKey="Schwemmle, Martin" sort="Schwemmle, Martin" uniqKey="Schwemmle M" first="Martin" last="Schwemmle">Martin Schwemmle</name><name sortKey="Sorgeloos, Frederic" sort="Sorgeloos, Frederic" uniqKey="Sorgeloos F" first="Frederic" last="Sorgeloos">Frederic Sorgeloos</name><name sortKey="Staeheli, Peter" sort="Staeheli, Peter" uniqKey="Staeheli P" first="Peter" last="Staeheli">Peter Staeheli</name></noCountry><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Mordstein, Markus" sort="Mordstein, Markus" uniqKey="Mordstein M" first="Markus" last="Mordstein">Markus Mordstein</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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