Lambda interferon renders epithelial cells of the respiratory and gastrointestinal tracts resistant to viral infections.
Identifieur interne : 002508 ( Main/Exploration ); précédent : 002507; suivant : 002509Lambda 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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Le document en format XML
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<author><name sortKey="Kochs, Georg" sort="Kochs, Georg" uniqKey="Kochs G" first="Georg" last="Kochs">Georg Kochs</name>
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<term>Epithelial Cells (virology)</term>
<term>Gastrointestinal Tract (immunology)</term>
<term>Gastrointestinal Tract (virology)</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Receptors, Interferon (deficiency)</term>
<term>Respiratory System (immunology)</term>
<term>Respiratory System (virology)</term>
<term>Virus Diseases (immunology)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Appareil respiratoire (immunologie)</term>
<term>Appareil respiratoire (virologie)</term>
<term>Cellules épithéliales (virologie)</term>
<term>Cytokines (immunologie)</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Maladies virales (immunologie)</term>
<term>Récepteur interféron (déficit)</term>
<term>Souris</term>
<term>Souris knockout</term>
<term>Tube digestif (immunologie)</term>
<term>Tube digestif (virologie)</term>
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<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptors, Interferon</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Appareil respiratoire</term>
<term>Cytokines</term>
<term>Maladies virales</term>
<term>Tube digestif</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Gastrointestinal Tract</term>
<term>Respiratory System</term>
<term>Virus Diseases</term>
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<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Appareil respiratoire</term>
<term>Cellules épithéliales</term>
<term>Tube digestif</term>
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<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Epithelial Cells</term>
<term>Gastrointestinal Tract</term>
<term>Respiratory System</term>
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<term>Immunité innée</term>
<term>Souris</term>
<term>Souris knockout</term>
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<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>
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<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>
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<country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Mordstein, Markus" sort="Mordstein, Markus" uniqKey="Mordstein M" first="Markus" last="Mordstein">Markus Mordstein</name>
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