Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells
Identifieur interne : 001F35 ( Ncbi/Curation ); précédent : 001F34; suivant : 001F36Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells
Auteurs : Helen Kw Law [République populaire de Chine] ; Chung Yan Cheung [République populaire de Chine] ; Sin Fun Sia [République populaire de Chine] ; Yuk On Chan [République populaire de Chine] ; Js Malik Peiris [République populaire de Chine] ; Yu Lung Lau [République populaire de Chine]Source :
- BMC Immunology [ 1471-2172 ] ; 2009.
Descripteurs français
- KwdFr :
- Adulte, Cellules cultivées, Cellules dendritiques (anatomopathologie), Cellules dendritiques (immunologie), Cellules dendritiques (métabolisme), Cellules dendritiques (virologie), Chine, Facteurs de l'âge, Femelle, Grossesse, Humains, Indice de gravité médicale, Ligand TRAIL (génétique), Ligand TRAIL (immunologie), Ligand TRAIL (métabolisme), Ligand de Fas (génétique), Ligand de Fas (immunologie), Ligand de Fas (métabolisme), Monocytes (anatomopathologie), Monocytes (métabolisme), Récepteur de type Toll-1 (génétique), Récepteur de type Toll-1 (immunologie), Récepteur de type Toll-1 (métabolisme), Récepteur de type Toll-10 (génétique), Récepteur de type Toll-10 (immunologie), Récepteur de type Toll-10 (métabolisme), Récepteurs CCR1 (génétique), Récepteurs CCR1 (immunologie), Récepteurs CCR1 (métabolisme), Récepteurs CCR3 (génétique), Récepteurs CCR3 (immunologie), Récepteurs CCR3 (métabolisme), Récepteurs CCR5 (génétique), Récepteurs CCR5 (immunologie), Récepteurs CCR5 (métabolisme), Régulation de l'expression des gènes (immunologie), Sang foetal, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (sang), Syndrome respiratoire aigu sévère (épidémiologie), Virulence (immunologie), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Cellules dendritiques, Monocytes.
- génétique : Ligand TRAIL, Ligand de Fas, Récepteur de type Toll-1, Récepteur de type Toll-10, Récepteurs CCR1, Récepteurs CCR3, Récepteurs CCR5.
- immunologie : Cellules dendritiques, Ligand TRAIL, Ligand de Fas, Récepteur de type Toll-1, Récepteur de type Toll-10, Récepteurs CCR1, Récepteurs CCR3, Récepteurs CCR5, Régulation de l'expression des gènes, Syndrome respiratoire aigu sévère, Virulence, Virus du SRAS.
- métabolisme : Cellules dendritiques, Ligand TRAIL, Ligand de Fas, Monocytes, Récepteur de type Toll-1, Récepteur de type Toll-10, Récepteurs CCR1, Récepteurs CCR3, Récepteurs CCR5.
- pathogénicité : Virus du SRAS.
- physiopathologie : Syndrome respiratoire aigu sévère.
- sang : Syndrome respiratoire aigu sévère.
- virologie : Cellules dendritiques.
- épidémiologie : Syndrome respiratoire aigu sévère.
- Adulte, Cellules cultivées, Chine, Facteurs de l'âge, Femelle, Grossesse, Humains, Indice de gravité médicale, Sang foetal.
- Wicri :
- geographic : République populaire de Chine.
English descriptors
- KwdEn :
- Adult, Age Factors, Cells, Cultured, China, Dendritic Cells (immunology), Dendritic Cells (metabolism), Dendritic Cells (pathology), Dendritic Cells (virology), Fas Ligand Protein (genetics), Fas Ligand Protein (immunology), Fas Ligand Protein (metabolism), Female, Fetal Blood, Gene Expression Regulation (immunology), Humans, Monocytes (metabolism), Monocytes (pathology), Pregnancy, Receptors, CCR1 (genetics), Receptors, CCR1 (immunology), Receptors, CCR1 (metabolism), Receptors, CCR3 (genetics), Receptors, CCR3 (immunology), Receptors, CCR3 (metabolism), Receptors, CCR5 (genetics), Receptors, CCR5 (immunology), Receptors, CCR5 (metabolism), SARS Virus (immunology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (blood), Severe Acute Respiratory Syndrome (epidemiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (physiopathology), Severity of Illness Index, TNF-Related Apoptosis-Inducing Ligand (genetics), TNF-Related Apoptosis-Inducing Ligand (immunology), TNF-Related Apoptosis-Inducing Ligand (metabolism), Toll-Like Receptor 1 (genetics), Toll-Like Receptor 1 (immunology), Toll-Like Receptor 1 (metabolism), Toll-Like Receptor 10 (genetics), Toll-Like Receptor 10 (immunology), Toll-Like Receptor 10 (metabolism), Virulence (immunology).
- MESH :
- chemical , genetics : Fas Ligand Protein, Receptors, CCR1, Receptors, CCR3, Receptors, CCR5, TNF-Related Apoptosis-Inducing Ligand, Toll-Like Receptor 1, Toll-Like Receptor 10.
- chemical , immunology : Fas Ligand Protein, Receptors, CCR1, Receptors, CCR3, Receptors, CCR5, TNF-Related Apoptosis-Inducing Ligand, Toll-Like Receptor 1, Toll-Like Receptor 10.
- chemical , metabolism : Fas Ligand Protein, Receptors, CCR1, Receptors, CCR3, Receptors, CCR5, TNF-Related Apoptosis-Inducing Ligand, Toll-Like Receptor 1, Toll-Like Receptor 10.
- geographic : China.
- blood : Severe Acute Respiratory Syndrome.
- epidemiology : Severe Acute Respiratory Syndrome.
- immunology : Dendritic Cells, Gene Expression Regulation, SARS Virus, Severe Acute Respiratory Syndrome, Virulence.
- metabolism : Dendritic Cells, Monocytes.
- pathogenicity : SARS Virus.
- pathology : Dendritic Cells, Monocytes.
- physiopathology : Severe Acute Respiratory Syndrome.
- virology : Dendritic Cells.
- Adult, Age Factors, Cells, Cultured, Female, Fetal Blood, Humans, Pregnancy, Severity of Illness Index.
Abstract
The SARS outbreak in 2003 provides a unique opportunity for the study of human responses to a novel virus. We have previously reported that dendritic cells (DCs) might be involved in the immune escape mechanisms for SARS-CoV. In this study, we focussed on the gene expression of toll-like receptors (TLRs), chemokine receptors (CCRs) and death receptor ligands in SARS-CoV infected DCs. We also compared adult and cord blood (CB) DCs to find a possible explanation for the age-dependent severity of SARS.
Our results demonstrates that SARS-CoV did not modulate TLR-1 to TLR-10 gene expression but significantly induced the expression of CCR-1, CCR-3, and CCR-5. There was also strong induction of TNF-related apoptosis-inducing ligand (TRAIL), but not Fas ligand gene expression in SARS-CoV infected DCs. Interestingly, the expressions of most genes studied were higher in CB DCs than adult DCs.
The upregulation of chemokines and CCRs may facilitate DC migration from the infection site to the lymph nodes, whereas the increase of TRAIL may induce lymphocyte apoptosis. These findings may explain the increased lung infiltrations and lymphoid depletion in SARS patients. Further explorations of the biological significance of these findings are warranted.
The online version of this article (doi:10.1186/1471-2172-10-35) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/1471-2172-10-35
PubMed: 19505311
PubMed Central: 2700820
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PMC:2700820Le document en format XML
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<term>Age Factors</term>
<term>Cells, Cultured</term>
<term>China</term>
<term>Dendritic Cells (immunology)</term>
<term>Dendritic Cells (metabolism)</term>
<term>Dendritic Cells (pathology)</term>
<term>Dendritic Cells (virology)</term>
<term>Fas Ligand Protein (genetics)</term>
<term>Fas Ligand Protein (immunology)</term>
<term>Fas Ligand Protein (metabolism)</term>
<term>Female</term>
<term>Fetal Blood</term>
<term>Gene Expression Regulation (immunology)</term>
<term>Humans</term>
<term>Monocytes (metabolism)</term>
<term>Monocytes (pathology)</term>
<term>Pregnancy</term>
<term>Receptors, CCR1 (genetics)</term>
<term>Receptors, CCR1 (immunology)</term>
<term>Receptors, CCR1 (metabolism)</term>
<term>Receptors, CCR3 (genetics)</term>
<term>Receptors, CCR3 (immunology)</term>
<term>Receptors, CCR3 (metabolism)</term>
<term>Receptors, CCR5 (genetics)</term>
<term>Receptors, CCR5 (immunology)</term>
<term>Receptors, CCR5 (metabolism)</term>
<term>SARS Virus (immunology)</term>
<term>SARS Virus (pathogenicity)</term>
<term>Severe Acute Respiratory Syndrome (blood)</term>
<term>Severe Acute Respiratory Syndrome (epidemiology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (physiopathology)</term>
<term>Severity of Illness Index</term>
<term>TNF-Related Apoptosis-Inducing Ligand (genetics)</term>
<term>TNF-Related Apoptosis-Inducing Ligand (immunology)</term>
<term>TNF-Related Apoptosis-Inducing Ligand (metabolism)</term>
<term>Toll-Like Receptor 1 (genetics)</term>
<term>Toll-Like Receptor 1 (immunology)</term>
<term>Toll-Like Receptor 1 (metabolism)</term>
<term>Toll-Like Receptor 10 (genetics)</term>
<term>Toll-Like Receptor 10 (immunology)</term>
<term>Toll-Like Receptor 10 (metabolism)</term>
<term>Virulence (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term>
<term>Cellules cultivées</term>
<term>Cellules dendritiques (anatomopathologie)</term>
<term>Cellules dendritiques (immunologie)</term>
<term>Cellules dendritiques (métabolisme)</term>
<term>Cellules dendritiques (virologie)</term>
<term>Chine</term>
<term>Facteurs de l'âge</term>
<term>Femelle</term>
<term>Grossesse</term>
<term>Humains</term>
<term>Indice de gravité médicale</term>
<term>Ligand TRAIL (génétique)</term>
<term>Ligand TRAIL (immunologie)</term>
<term>Ligand TRAIL (métabolisme)</term>
<term>Ligand de Fas (génétique)</term>
<term>Ligand de Fas (immunologie)</term>
<term>Ligand de Fas (métabolisme)</term>
<term>Monocytes (anatomopathologie)</term>
<term>Monocytes (métabolisme)</term>
<term>Récepteur de type Toll-1 (génétique)</term>
<term>Récepteur de type Toll-1 (immunologie)</term>
<term>Récepteur de type Toll-1 (métabolisme)</term>
<term>Récepteur de type Toll-10 (génétique)</term>
<term>Récepteur de type Toll-10 (immunologie)</term>
<term>Récepteur de type Toll-10 (métabolisme)</term>
<term>Récepteurs CCR1 (génétique)</term>
<term>Récepteurs CCR1 (immunologie)</term>
<term>Récepteurs CCR1 (métabolisme)</term>
<term>Récepteurs CCR3 (génétique)</term>
<term>Récepteurs CCR3 (immunologie)</term>
<term>Récepteurs CCR3 (métabolisme)</term>
<term>Récepteurs CCR5 (génétique)</term>
<term>Récepteurs CCR5 (immunologie)</term>
<term>Récepteurs CCR5 (métabolisme)</term>
<term>Régulation de l'expression des gènes (immunologie)</term>
<term>Sang foetal</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (physiopathologie)</term>
<term>Syndrome respiratoire aigu sévère (sang)</term>
<term>Syndrome respiratoire aigu sévère (épidémiologie)</term>
<term>Virulence (immunologie)</term>
<term>Virus du SRAS (immunologie)</term>
<term>Virus du SRAS (pathogénicité)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fas Ligand Protein</term>
<term>Receptors, CCR1</term>
<term>Receptors, CCR3</term>
<term>Receptors, CCR5</term>
<term>TNF-Related Apoptosis-Inducing Ligand</term>
<term>Toll-Like Receptor 1</term>
<term>Toll-Like Receptor 10</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Fas Ligand Protein</term>
<term>Receptors, CCR1</term>
<term>Receptors, CCR3</term>
<term>Receptors, CCR5</term>
<term>TNF-Related Apoptosis-Inducing Ligand</term>
<term>Toll-Like Receptor 1</term>
<term>Toll-Like Receptor 10</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fas Ligand Protein</term>
<term>Receptors, CCR1</term>
<term>Receptors, CCR3</term>
<term>Receptors, CCR5</term>
<term>TNF-Related Apoptosis-Inducing Ligand</term>
<term>Toll-Like Receptor 1</term>
<term>Toll-Like Receptor 10</term>
</keywords>
<keywords scheme="MESH" type="geographic" xml:lang="en"><term>China</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Monocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Ligand TRAIL</term>
<term>Ligand de Fas</term>
<term>Récepteur de type Toll-1</term>
<term>Récepteur de type Toll-10</term>
<term>Récepteurs CCR1</term>
<term>Récepteurs CCR3</term>
<term>Récepteurs CCR5</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Ligand TRAIL</term>
<term>Ligand de Fas</term>
<term>Récepteur de type Toll-1</term>
<term>Récepteur de type Toll-10</term>
<term>Récepteurs CCR1</term>
<term>Récepteurs CCR3</term>
<term>Récepteurs CCR5</term>
<term>Régulation de l'expression des gènes</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Virulence</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dendritic Cells</term>
<term>Gene Expression Regulation</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dendritic Cells</term>
<term>Monocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Ligand TRAIL</term>
<term>Ligand de Fas</term>
<term>Monocytes</term>
<term>Récepteur de type Toll-1</term>
<term>Récepteur de type Toll-10</term>
<term>Récepteurs CCR1</term>
<term>Récepteurs CCR3</term>
<term>Récepteurs CCR5</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dendritic Cells</term>
<term>Monocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Cellules dendritiques</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Dendritic Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Age Factors</term>
<term>Cells, Cultured</term>
<term>Female</term>
<term>Fetal Blood</term>
<term>Humans</term>
<term>Pregnancy</term>
<term>Severity of Illness Index</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte</term>
<term>Cellules cultivées</term>
<term>Chine</term>
<term>Facteurs de l'âge</term>
<term>Femelle</term>
<term>Grossesse</term>
<term>Humains</term>
<term>Indice de gravité médicale</term>
<term>Sang foetal</term>
</keywords>
<keywords scheme="Wicri" type="geographic" xml:lang="fr"><term>République populaire de Chine</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>The SARS outbreak in 2003 provides a unique opportunity for the study of human responses to a novel virus. We have previously reported that dendritic cells (DCs) might be involved in the immune escape mechanisms for SARS-CoV. In this study, we focussed on the gene expression of toll-like receptors (TLRs), chemokine receptors (CCRs) and death receptor ligands in SARS-CoV infected DCs. We also compared adult and cord blood (CB) DCs to find a possible explanation for the age-dependent severity of SARS.</p>
</sec>
<sec><title>Results</title>
<p>Our results demonstrates that SARS-CoV did not modulate TLR-1 to TLR-10 gene expression but significantly induced the expression of CCR-1, CCR-3, and CCR-5. There was also strong induction of TNF-related apoptosis-inducing ligand (TRAIL), but not Fas ligand gene expression in SARS-CoV infected DCs. Interestingly, the expressions of most genes studied were higher in CB DCs than adult DCs.</p>
</sec>
<sec><title>Conclusion</title>
<p>The upregulation of chemokines and CCRs may facilitate DC migration from the infection site to the lymph nodes, whereas the increase of TRAIL may induce lymphocyte apoptosis. These findings may explain the increased lung infiltrations and lymphoid depletion in SARS patients. Further explorations of the biological significance of these findings are warranted.</p>
</sec>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1186/1471-2172-10-35) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
</front>
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