Chemokine up-regulation in SARS-coronavirus -infected, monocyte-derived human dendritic cells
Identifieur interne : 000690 ( PascalFrancis/Checkpoint ); précédent : 000689; suivant : 000691Chemokine up-regulation in SARS-coronavirus -infected, monocyte-derived human dendritic cells
Auteurs : Helen K. W. Law [Hong Kong] ; CHUNG YAN CHEUNG ; HOI YEE NG ; SIN FUN SIA ; YUK ON CHAN ; Winsie Luk ; John M. Nicholls ; J. S. Malik Peiris ; YU LUNG LAUSource :
- Blood [ 0006-4971 ] ; 2005.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
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Abstract
Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). In this study, we focused on dendritic cells (DCs) which play important roles in linking the innate and adaptive immunity. SARS-CoV was shown to infect both immature and mature human monocyte-derived DCs by electron microscopy and immunofluorescence. The detection of negative strands of SARS-CoV RNA in DCs suggested viral replication. However, no increase in viral RNA was observed. Using cytopathic assays, no increase in virus titer was detected in infected DCs and cell-culture supernatant, confirming that virus replication was incomplete. No induction of apoptosis or maturation was detected in SARS-CoV-infected DCs. The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon a [IFN-a], IFN-β, IFN-γ, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor a [TNF-α] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1α [MIP-1α], regulated on activation normal T cell expressed and secreted [RANTES]), interferon-inducible protein of 10 kDa [IP-10], and monocyte chemo-attractant protein 1 [MCP-1]). The lack of antiviral cytokine response against a background of intense chemokine up-regulation could represent a mechanism of immune evasion by SARS-CoV.
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Law</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Paediatrics and Adolescent Medicine, the Department of Microbiology, and the Department of Pathology, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital</s1><s2>Pokfulam</s2><s3>HKG</s3></inist:fA14><country>Hong Kong</country><wicri:noRegion>Pokfulam</wicri:noRegion></affiliation></author><author><name sortKey="Chung Yan Cheung" sort="Chung Yan Cheung" uniqKey="Chung Yan Cheung" last="Chung Yan Cheung">CHUNG YAN CHEUNG</name></author><author><name sortKey="Hoi Yee Ng" sort="Hoi Yee Ng" uniqKey="Hoi Yee Ng" last="Hoi Yee Ng">HOI YEE NG</name></author><author><name sortKey="Sin Fun Sia" sort="Sin Fun Sia" uniqKey="Sin Fun Sia" last="Sin Fun Sia">SIN FUN SIA</name></author><author><name sortKey="Yuk On Chan" sort="Yuk On Chan" uniqKey="Yuk On Chan" last="Yuk On Chan">YUK ON CHAN</name></author><author><name sortKey="Luk, Winsie" sort="Luk, Winsie" uniqKey="Luk W" first="Winsie" last="Luk">Winsie Luk</name></author><author><name sortKey="Nicholls, John M" sort="Nicholls, John M" uniqKey="Nicholls J" first="John M." last="Nicholls">John M. 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Law</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Paediatrics and Adolescent Medicine, the Department of Microbiology, and the Department of Pathology, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital</s1><s2>Pokfulam</s2><s3>HKG</s3></inist:fA14><country>Hong Kong</country><wicri:noRegion>Pokfulam</wicri:noRegion></affiliation></author><author><name sortKey="Chung Yan Cheung" sort="Chung Yan Cheung" uniqKey="Chung Yan Cheung" last="Chung Yan Cheung">CHUNG YAN CHEUNG</name></author><author><name sortKey="Hoi Yee Ng" sort="Hoi Yee Ng" uniqKey="Hoi Yee Ng" last="Hoi Yee Ng">HOI YEE NG</name></author><author><name sortKey="Sin Fun Sia" sort="Sin Fun Sia" uniqKey="Sin Fun Sia" last="Sin Fun Sia">SIN FUN SIA</name></author><author><name sortKey="Yuk On Chan" sort="Yuk On Chan" uniqKey="Yuk On Chan" last="Yuk On Chan">YUK ON CHAN</name></author><author><name sortKey="Luk, Winsie" sort="Luk, Winsie" uniqKey="Luk W" first="Winsie" last="Luk">Winsie Luk</name></author><author><name sortKey="Nicholls, John M" sort="Nicholls, John M" uniqKey="Nicholls J" first="John M." last="Nicholls">John M. Nicholls</name></author><author><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J. S. Malik" last="Peiris">J. S. Malik Peiris</name></author><author><name sortKey="Yu Lung Lau" sort="Yu Lung Lau" uniqKey="Yu Lung Lau" last="Yu Lung Lau">YU LUNG LAU</name></author></analytic><series><title level="j" type="main">Blood</title><title level="j" type="abbreviated">Blood</title><idno type="ISSN">0006-4971</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Blood</title><title level="j" type="abbreviated">Blood</title><idno type="ISSN">0006-4971</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigen presenting cell</term><term>Chemokine</term><term>Coronavirus</term><term>Dendritic cell</term><term>Human</term><term>Immune evasion</term><term>Immune response</term><term>Infected cell</term><term>Monocyte</term><term>Severe acute respiratory syndrome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Chimiokine</term><term>Coronavirus</term><term>Cellule infectée</term><term>Syndrome respiratoire aigu sévère</term><term>Monocyte</term><term>Homme</term><term>Cellule dendritique</term><term>Cellule APC</term><term>Immunosubversion</term><term>Réponse immune</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). In this study, we focused on dendritic cells (DCs) which play important roles in linking the innate and adaptive immunity. SARS-CoV was shown to infect both immature and mature human monocyte-derived DCs by electron microscopy and immunofluorescence. The detection of negative strands of SARS-CoV RNA in DCs suggested viral replication. However, no increase in viral RNA was observed. Using cytopathic assays, no increase in virus titer was detected in infected DCs and cell-culture supernatant, confirming that virus replication was incomplete. No induction of apoptosis or maturation was detected in SARS-CoV-infected DCs. The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon a [IFN-a], IFN-β, IFN-γ, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor a [TNF-α] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1α [MIP-1α], regulated on activation normal T cell expressed and secreted [RANTES]), interferon-inducible protein of 10 kDa [IP-10], and monocyte chemo-attractant protein 1 [MCP-1]). The lack of antiviral cytokine response against a background of intense chemokine up-regulation could represent a mechanism of immune evasion by SARS-CoV.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-4971</s0></fA01><fA03 i2="1"><s0>Blood</s0></fA03><fA05><s2>106</s2></fA05><fA06><s2>7</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Chemokine up-regulation in SARS-coronavirus -infected, monocyte-derived human dendritic cells</s1></fA08><fA11 i1="01" i2="1"><s1>LAW (Helen K. W.)</s1></fA11><fA11 i1="02" i2="1"><s1>CHUNG YAN CHEUNG</s1></fA11><fA11 i1="03" i2="1"><s1>HOI YEE NG</s1></fA11><fA11 i1="04" i2="1"><s1>SIN FUN SIA</s1></fA11><fA11 i1="05" i2="1"><s1>YUK ON CHAN</s1></fA11><fA11 i1="06" i2="1"><s1>LUK (Winsie)</s1></fA11><fA11 i1="07" i2="1"><s1>NICHOLLS (John M.)</s1></fA11><fA11 i1="08" i2="1"><s1>PEIRIS (J. S. Malik)</s1></fA11><fA11 i1="09" i2="1"><s1>YU LUNG LAU</s1></fA11><fA14 i1="01"><s1>Department of Paediatrics and Adolescent Medicine, the Department of Microbiology, and the Department of Pathology, Hong Kong Jockey Club Clinical Research Centre, Faculty of Medicine, The University of Hong Kong, Queen Mary Hospital</s1><s2>Pokfulam</s2><s3>HKG</s3></fA14><fA20><s1>2366-2374</s1></fA20><fA21><s1>2005</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>3178</s2><s5>354000132785290190</s5></fA43><fA44><s0>0000</s0><s1>© 2006 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>59 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>06-0102714</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Blood</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Lymphopenia and increasing viral load in the first 10 days of severe acute respiratory syndrome (SARS) suggested immune evasion by SARS-coronavirus (CoV). 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The SARS-CoV-infected DCs showed low expression of antiviral cytokines (interferon a [IFN-a], IFN-β, IFN-γ, and interleukin 12p40 [IL-12p40]), moderate up-regulation of proinflammatory cytokines (tumor necrosis factor a [TNF-α] and IL-6) but significant up-regulation of inflammatory chemokines (macrophage inflammatory protein 1α [MIP-1α], regulated on activation normal T cell expressed and secreted [RANTES]), interferon-inducible protein of 10 kDa [IP-10], and monocyte chemo-attractant protein 1 [MCP-1]). 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Nicholls</name><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J. S. Malik" last="Peiris">J. S. Malik Peiris</name><name sortKey="Sin Fun Sia" sort="Sin Fun Sia" uniqKey="Sin Fun Sia" last="Sin Fun Sia">SIN FUN SIA</name><name sortKey="Yu Lung Lau" sort="Yu Lung Lau" uniqKey="Yu Lung Lau" last="Yu Lung Lau">YU LUNG LAU</name><name sortKey="Yuk On Chan" sort="Yuk On Chan" uniqKey="Yuk On Chan" last="Yuk On Chan">YUK ON CHAN</name></noCountry><country name="Hong Kong"><noRegion><name sortKey="Law, Helen K W" sort="Law, Helen K W" uniqKey="Law H" first="Helen K. W." last="Law">Helen K. W. Law</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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