SrasV1, PascalFrancis, Corpus, bibRecord, 000390

Control of coronavirus infection through plasmacytoid dendritic-cell-derived type I interferon

Identifieur interne : 000390 ( PascalFrancis/Corpus ); précédent : 000389; suivant : 000391

Control of coronavirus infection through plasmacytoid dendritic-cell-derived type I interferon

Auteurs : Luisa Cervantes Barragan ; Roland Zust ; Friedemann Weber ; Martin Spiegel ; Karl S. Lang ; Shizuo Akira ; Volker Thiel ; Burkhard Ludewig

Source :

Blood [ 0006-4971 ] ; 2007.

RBID : Pascal:07-0181449

Descripteurs français

Pascal (Inist)
- Infection, Coronavirus, Cellule dendritique, Syndrome respiratoire aigu sévère, Récepteur cellule T, Virus hépatite murine, Interféron alpha, Interféron bêta, Souris, Homme, Culture primaire, Cellule dendritique plasmocytoïde.

English descriptors

KwdEn :
- Alpha interferon, Beta interferon, Coronavirus, Dendritic cell, Human, Infection, Mouse, Murine hepatitis virus, Plasmacytoid dendritic cell, Primary culture, Severe acute respiratory syndrome, T cell receptor.

Abstract

This study demonstrates a unique and crucial role of plasmacytoid dendritic cells (pDCs) and pDC-derived type I interferons (IFNs) in the pathogenesis of mouse coronavirus infection. pDCs controlled the fast replicating mouse hepatitis virus (MHV) through the immediate production of type I IFNs. Recognition of MHV by pDCs was mediated via TLR7 ensuring a swift IFN-a production following encounter with this cytopathic RNA virus. Furthermore, the particular type I IFN response pattern was not restricted to the murine coronavirus, but was also found in infection with the highly cytopathic human severe acute respiratory syndrome (SARS) coronavirus. Taken together, our results suggest that rapid production of type I IFNs by pDCs is essential for the control of potentially lethal coronavirus infections.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 07-0181449 LBEI
ET :	Control of coronavirus infection through plasmacytoid dendritic-cell-derived type I interferon
AU :	CERVANTES -BARRAGAN (Luisa); ZUST (Roland); WEBER (Friedemann); SPIEGEL (Martin); LANG (Karl S.); AKIRA (Shizuo); THIEL (Volker); LUDEWIG (Burkhard)
AF :	Research Department, Kantonal Hospital St Gallen/St Gallen/Suisse (1 aut., 2 aut., 7 aut., 8 aut.); Unidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades/Mexico City/Mexique (1 aut.); Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg/Freiburg/Allemagne (3 aut., 4 aut.); Institute of Experimental Immunology, University Hospital/Zurich/Suisse (5 aut.); Department of Host Defense, Osaka University/Osaka/Japon (6 aut.)
DT :	Publication en série; Niveau analytique
SO :	Blood; ISSN 0006-4971; Etats-Unis; Da. 2007; Vol. 109; No. 3; Pp. 1131-1137; Bibl. 54 ref.
LA :	Anglais
EA :	This study demonstrates a unique and crucial role of plasmacytoid dendritic cells (pDCs) and pDC-derived type I interferons (IFNs) in the pathogenesis of mouse coronavirus infection. pDCs controlled the fast replicating mouse hepatitis virus (MHV) through the immediate production of type I IFNs. Recognition of MHV by pDCs was mediated via TLR7 ensuring a swift IFN-a production following encounter with this cytopathic RNA virus. Furthermore, the particular type I IFN response pattern was not restricted to the murine coronavirus, but was also found in infection with the highly cytopathic human severe acute respiratory syndrome (SARS) coronavirus. Taken together, our results suggest that rapid production of type I IFNs by pDCs is essential for the control of potentially lethal coronavirus infections.
CC :	002B05C02C
FD :	Infection; Coronavirus; Cellule dendritique; Syndrome respiratoire aigu sévère; Récepteur cellule T; Virus hépatite murine; Interféron alpha; Interféron bêta; Souris; Homme; Culture primaire; Cellule dendritique plasmocytoïde
FG :	Coronaviridae; Nidovirales; Virus; Virose; Rodentia; Mammalia; Vertebrata; Cytokine
ED :	Infection; Coronavirus; Dendritic cell; Severe acute respiratory syndrome; T cell receptor; Murine hepatitis virus; Alpha interferon; Beta interferon; Mouse; Human; Primary culture; Plasmacytoid dendritic cell
EG :	Coronaviridae; Nidovirales; Virus; Viral disease; Rodentia; Mammalia; Vertebrata; Cytokine
SD :	Infección; Coronavirus; Célula dendrítica; Síndrome respiratorio agudo severo; Receptor célula T; Murine hepatitis virus; Interferón alfa; Interferón beta; Ratón; Hombre; Cultivo primario
LO :	INIST-3178.354000159350010350
ID :	07-0181449

Links to Exploration step

Pascal:07-0181449

Le document en format XML

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<front><div type="abstract" xml:lang="en">This study demonstrates a unique and crucial role of plasmacytoid dendritic cells (pDCs) and pDC-derived type I interferons (IFNs) in the pathogenesis of mouse coronavirus infection. pDCs controlled the fast replicating mouse hepatitis virus (MHV) through the immediate production of type I IFNs. Recognition of MHV by pDCs was mediated via TLR7 ensuring a swift IFN-a production following encounter with this cytopathic RNA virus. Furthermore, the particular type I IFN response pattern was not restricted to the murine coronavirus, but was also found in infection with the highly cytopathic human severe acute respiratory syndrome (SARS) coronavirus. Taken together, our results suggest that rapid production of type I IFNs by pDCs is essential for the control of potentially lethal coronavirus infections.</div>
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<fA11 i1="06" i2="1"><s1>AKIRA (Shizuo)</s1>
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<fA11 i1="07" i2="1"><s1>THIEL (Volker)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>LUDEWIG (Burkhard)</s1>
</fA11>
<fA14 i1="01"><s1>Research Department, Kantonal Hospital St Gallen</s1>
<s2>St Gallen</s2>
<s3>CHE</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Unidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades</s1>
<s2>Mexico City</s2>
<s3>MEX</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg</s1>
<s2>Freiburg</s2>
<s3>DEU</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Institute of Experimental Immunology, University Hospital</s1>
<s2>Zurich</s2>
<s3>CHE</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Host Defense, Osaka University</s1>
<s2>Osaka</s2>
<s3>JPN</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>1131-1137</s1>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
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</fA45>
<fA47 i1="01" i2="1"><s0>07-0181449</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
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<fA64 i1="01" i2="1"><s0>Blood</s0>
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</fA66>
<fC01 i1="01" l="ENG"><s0>This study demonstrates a unique and crucial role of plasmacytoid dendritic cells (pDCs) and pDC-derived type I interferons (IFNs) in the pathogenesis of mouse coronavirus infection. pDCs controlled the fast replicating mouse hepatitis virus (MHV) through the immediate production of type I IFNs. Recognition of MHV by pDCs was mediated via TLR7 ensuring a swift IFN-a production following encounter with this cytopathic RNA virus. Furthermore, the particular type I IFN response pattern was not restricted to the murine coronavirus, but was also found in infection with the highly cytopathic human severe acute respiratory syndrome (SARS) coronavirus. Taken together, our results suggest that rapid production of type I IFNs by pDCs is essential for the control of potentially lethal coronavirus infections.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B05C02C</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Infection</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Infection</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Infección</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>02</s5>
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<s5>03</s5>
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<s5>03</s5>
</fC03>
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<s5>03</s5>
</fC03>
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<s2>NM</s2>
<s5>04</s5>
</fC03>
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<s2>NM</s2>
<s5>04</s5>
</fC03>
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<s2>NM</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Récepteur cellule T</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>T cell receptor</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Receptor célula T</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Virus hépatite murine</s0>
<s2>NW</s2>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Murine hepatitis virus</s0>
<s2>NW</s2>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Murine hepatitis virus</s0>
<s2>NW</s2>
<s5>07</s5>
</fC03>
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<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Alpha interferon</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Interferón alfa</s0>
<s5>08</s5>
</fC03>
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<s5>09</s5>
</fC03>
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<s5>09</s5>
</fC03>
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<s5>09</s5>
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<fC03 i1="09" i2="X" l="FRE"><s0>Souris</s0>
<s5>17</s5>
</fC03>
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<s5>17</s5>
</fC03>
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<s5>17</s5>
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<s5>18</s5>
</fC03>
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<s5>18</s5>
</fC03>
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<s5>18</s5>
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<s5>19</s5>
</fC03>
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<s5>19</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Cellule dendritique plasmocytoïde</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Plasmacytoid dendritic cell</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>37</s5>
</fC07>
<fN21><s1>122</s1>
</fN21>
<fN44 i1="01"><s1>PSI</s1>
</fN44>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 07-0181449 LBEI</NO>
<ET>Control of coronavirus infection through plasmacytoid dendritic-cell-derived type I interferon</ET>
<AU>CERVANTES -BARRAGAN (Luisa); ZUST (Roland); WEBER (Friedemann); SPIEGEL (Martin); LANG (Karl S.); AKIRA (Shizuo); THIEL (Volker); LUDEWIG (Burkhard)</AU>
<AF>Research Department, Kantonal Hospital St Gallen/St Gallen/Suisse (1 aut., 2 aut., 7 aut., 8 aut.); Unidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades/Mexico City/Mexique (1 aut.); Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg/Freiburg/Allemagne (3 aut., 4 aut.); Institute of Experimental Immunology, University Hospital/Zurich/Suisse (5 aut.); Department of Host Defense, Osaka University/Osaka/Japon (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Blood; ISSN 0006-4971; Etats-Unis; Da. 2007; Vol. 109; No. 3; Pp. 1131-1137; Bibl. 54 ref.</SO>
<LA>Anglais</LA>
<EA>This study demonstrates a unique and crucial role of plasmacytoid dendritic cells (pDCs) and pDC-derived type I interferons (IFNs) in the pathogenesis of mouse coronavirus infection. pDCs controlled the fast replicating mouse hepatitis virus (MHV) through the immediate production of type I IFNs. Recognition of MHV by pDCs was mediated via TLR7 ensuring a swift IFN-a production following encounter with this cytopathic RNA virus. Furthermore, the particular type I IFN response pattern was not restricted to the murine coronavirus, but was also found in infection with the highly cytopathic human severe acute respiratory syndrome (SARS) coronavirus. Taken together, our results suggest that rapid production of type I IFNs by pDCs is essential for the control of potentially lethal coronavirus infections.</EA>
<CC>002B05C02C</CC>
<FD>Infection; Coronavirus; Cellule dendritique; Syndrome respiratoire aigu sévère; Récepteur cellule T; Virus hépatite murine; Interféron alpha; Interféron bêta; Souris; Homme; Culture primaire; Cellule dendritique plasmocytoïde</FD>
<FG>Coronaviridae; Nidovirales; Virus; Virose; Rodentia; Mammalia; Vertebrata; Cytokine</FG>
<ED>Infection; Coronavirus; Dendritic cell; Severe acute respiratory syndrome; T cell receptor; Murine hepatitis virus; Alpha interferon; Beta interferon; Mouse; Human; Primary culture; Plasmacytoid dendritic cell</ED>
<EG>Coronaviridae; Nidovirales; Virus; Viral disease; Rodentia; Mammalia; Vertebrata; Cytokine</EG>
<SD>Infección; Coronavirus; Célula dendrítica; Síndrome respiratorio agudo severo; Receptor célula T; Murine hepatitis virus; Interferón alfa; Interferón beta; Ratón; Hombre; Cultivo primario</SD>
<LO>INIST-3178.354000159350010350</LO>
<ID>07-0181449</ID>
</server>
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Control of coronavirus infection through plasmacytoid dendritic-cell-derived type I interferon

Control of coronavirus infection through plasmacytoid dendritic-cell-derived type I interferon

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