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Article: Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells
Title | Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells | ||||||||
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Authors | |||||||||
Issue Date | 2009 | ||||||||
Publisher | BioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcimmunol/ | ||||||||
Citation | Bmc Immunology, 2009, v. 10 How to Cite? | ||||||||
Abstract | Background: 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. Results: 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. Conclusion: 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. © 2009 Law et al; licensee BioMed Central Ltd. | ||||||||
Persistent Identifier | http://hdl.handle.net/10722/59389 | ||||||||
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 0.815 | ||||||||
PubMed Central ID | |||||||||
ISI Accession Number ID |
Funding Information: The authors thank the staff of Department of Microbiology, The University of Hong Kong for their technical support; and the staff of labor ward, Queen Mary Hospital, in facilitating the collection of cord blood. The work described in this paper is supported partially by the Special SARS Research Fund and the Outstanding Researcher Award (YLL, JSMP) from the University of Hong Kong; the Public Health Research Grant (AI 95357) from the National Institute of Allergy and Infectious Diseases, USA and the Research Fund for the Control of Infectious Diseases (RFCID 03040772) from the HKSAR Government. We also thank Dr. Matthew Buckwalter, Insitut Pasteur, France for proofreading the manuscript. | ||||||||
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Law, HKW | en_HK |
dc.contributor.author | Cheung, CY | en_HK |
dc.contributor.author | Sia, SF | en_HK |
dc.contributor.author | Chan, YO | en_HK |
dc.contributor.author | Peiris, JSM | en_HK |
dc.contributor.author | Lau, YL | en_HK |
dc.date.accessioned | 2010-05-31T03:49:06Z | - |
dc.date.available | 2010-05-31T03:49:06Z | - |
dc.date.issued | 2009 | en_HK |
dc.identifier.citation | Bmc Immunology, 2009, v. 10 | en_HK |
dc.identifier.issn | 1471-2172 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/59389 | - |
dc.description.abstract | Background: 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. Results: 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. Conclusion: 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. © 2009 Law et al; licensee BioMed Central Ltd. | en_HK |
dc.language | eng | en_HK |
dc.publisher | BioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcimmunol/ | en_HK |
dc.relation.ispartof | BMC Immunology | en_HK |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.rights | B M C Immunology. Copyright © BioMed Central Ltd. | en_HK |
dc.subject.mesh | Dendritic Cells - immunology - metabolism - pathology - virology | - |
dc.subject.mesh | Receptors, CCR1 - genetics - immunology - metabolism | - |
dc.subject.mesh | Receptors, CCR3 - genetics - immunology - metabolism | - |
dc.subject.mesh | Receptors, CCR5 - genetics - immunology - metabolism | - |
dc.subject.mesh | SARS Virus - immunology - pathogenicity | - |
dc.title | Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1471-2172&volume=10&issue=35&spage=&epage=&date=2009&atitle=Toll-like+receptors,+chemokine+receptors+and+death+receptor+ligands+responses+in+SARS+coronavirus+infected+human+monocyte+derived+dendritic+cells | en_HK |
dc.identifier.email | Cheung, CY: chungey@hkucc.hku.hk | en_HK |
dc.identifier.email | Peiris, JSM: malik@hkucc.hku.hk | en_HK |
dc.identifier.email | Lau, YL: lauylung@hku.hk | en_HK |
dc.identifier.authority | Cheung, CY=rp00404 | en_HK |
dc.identifier.authority | Peiris, JSM=rp00410 | en_HK |
dc.identifier.authority | Lau, YL=rp00361 | en_HK |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1186/1471-2172-10-35 | en_HK |
dc.identifier.pmid | 19505311 | - |
dc.identifier.pmcid | PMC2700820 | - |
dc.identifier.scopus | eid_2-s2.0-67649887153 | en_HK |
dc.identifier.hkuros | 164803 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-67649887153&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 10 | en_HK |
dc.identifier.issue | 35 | - |
dc.identifier.isi | WOS:000267746900001 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Law, HKW=7101939394 | en_HK |
dc.identifier.scopusauthorid | Cheung, CY=7202061836 | en_HK |
dc.identifier.scopusauthorid | Sia, SF=8574447900 | en_HK |
dc.identifier.scopusauthorid | Chan, YO=55065554600 | en_HK |
dc.identifier.scopusauthorid | Peiris, JSM=7005486823 | en_HK |
dc.identifier.scopusauthorid | Lau, YL=7201403380 | en_HK |
dc.identifier.citeulike | 4841273 | - |
dc.identifier.issnl | 1471-2172 | - |