Interferon interplay helps tissue cells to cope with SARS-coronavirus infection.
Identifieur interne : 006735 ( Main/Exploration ); précédent : 006734; suivant : 006736Interferon interplay helps tissue cells to cope with SARS-coronavirus infection.
Auteurs : Thomas Kuri [Allemagne] ; Friedemann WeberSource :
- Virulence [ 2150-5608 ]
Descripteurs français
- KwdFr :
- Animaux, Cellules dendritiques (cytologie), Cellules dendritiques (immunologie), Cellules dendritiques (métabolisme), Facteur-3 de régulation d'interféron (métabolisme), Facteur-7 de régulation d'interféron (métabolisme), Humains, Immunité innée, Interféron de type I (biosynthèse), Interféron de type I (immunologie), Interféron de type I (pharmacologie), Lignée cellulaire, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- biosynthèse : Interféron de type I.
- cytologie : Cellules dendritiques.
- immunologie : Cellules dendritiques, Interféron de type I, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Cellules dendritiques, Facteur-3 de régulation d'interféron, Facteur-7 de régulation d'interféron.
- pathogénicité : Virus du SRAS.
- pharmacologie : Interféron de type I.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Humains, Immunité innée, Lignée cellulaire.
English descriptors
- KwdEn :
- Animals, Cell Line, Dendritic Cells (cytology), Dendritic Cells (immunology), Dendritic Cells (metabolism), Humans, Immunity, Innate, Interferon Regulatory Factor-3 (metabolism), Interferon Regulatory Factor-7 (metabolism), Interferon Type I (biosynthesis), Interferon Type I (immunology), Interferon Type I (pharmacology), SARS Virus (immunology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- chemical , biosynthesis : Interferon Type I.
- chemical , immunology : Interferon Type I.
- chemical , metabolism : Interferon Regulatory Factor-3, Interferon Regulatory Factor-7.
- cytology : Dendritic Cells.
- immunology : Dendritic Cells, SARS Virus, Severe Acute Respiratory Syndrome.
- metabolism : Dendritic Cells.
- pathogenicity : SARS Virus.
- chemical , pharmacology : Interferon Type I.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Humans, Immunity, Innate.
Abstract
SARS coronavirus (SARS-CoV), the causative agent of severe acute respiratory syndrome, is a versatile pathogen armed with a host of factors countering the antiviral type I interferon (IFN) system. Hence, tissue cells infected with SARS-CoV are unable to launch an IFN response. Plasmacytoid dendritic cells, however, produce high levels of IFN after infection. We recently demonstrated that minute amounts of IFN applied before infection (IFN priming) can ameliorate the IFN response of tissue cells to SARS-CoV. IFN priming of SARS-CoV-infected cells activated genes for IFN transcription, IFN signaling, antiviral effector proteins, ubiquitinylation and ISGylation, antigen presentation, and other cytokines and chemokines, whereas IFN treatment or infection alone had no major effect. Thus, the IFN which is produced by plasmacytoid dendritic cells could enable tissue cells to at least partially overturn the SARS-CoV-induced block in innate immune activation.
DOI: 10.4161/viru.1.4.11465
PubMed: 21178452
Affiliations:
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xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Immunité innée</term><term>Lignée cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">SARS coronavirus (SARS-CoV), the causative agent of severe acute respiratory syndrome, is a versatile pathogen armed with a host of factors countering the antiviral type I interferon (IFN) system. Hence, tissue cells infected with SARS-CoV are unable to launch an IFN response. Plasmacytoid dendritic cells, however, produce high levels of IFN after infection. We recently demonstrated that minute amounts of IFN applied before infection (IFN priming) can ameliorate the IFN response of tissue cells to SARS-CoV. IFN priming of SARS-CoV-infected cells activated genes for IFN transcription, IFN signaling, antiviral effector proteins, ubiquitinylation and ISGylation, antigen presentation, and other cytokines and chemokines, whereas IFN treatment or infection alone had no major effect. Thus, the IFN which is produced by plasmacytoid dendritic cells could enable tissue cells to at least partially overturn the SARS-CoV-induced block in innate immune activation.</div></front></TEI><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="Weber, Friedemann" sort="Weber, Friedemann" uniqKey="Weber F" first="Friedemann" last="Weber">Friedemann Weber</name></noCountry><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Kuri, Thomas" sort="Kuri, Thomas" uniqKey="Kuri T" first="Thomas" last="Kuri">Thomas Kuri</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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