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Article: Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells

TitleToll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells
Authors
Issue Date2009
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcimmunol/
Citation
Bmc Immunology, 2009, v. 10 How to Cite?
AbstractBackground: 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 Identifierhttp://hdl.handle.net/10722/59389
ISSN
2015 Impact Factor: 2.161
2015 SCImago Journal Rankings: 1.087
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
National Institute of Allergy and Infectious Diseases, USAAI 95357
HKSAR GovernmentRFCID 03040772
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 FieldValueLanguage
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorCheung, CYen_HK
dc.contributor.authorSia, SFen_HK
dc.contributor.authorChan, YOen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-05-31T03:49:06Z-
dc.date.available2010-05-31T03:49:06Z-
dc.date.issued2009en_HK
dc.identifier.citationBmc Immunology, 2009, v. 10en_HK
dc.identifier.issn1471-2172en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59389-
dc.description.abstractBackground: 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.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcimmunol/en_HK
dc.relation.ispartofBMC Immunologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsB M C Immunology. Copyright © BioMed Central Ltd.en_HK
dc.subject.meshDendritic Cells - immunology - metabolism - pathology - virology-
dc.subject.meshReceptors, CCR1 - genetics - immunology - metabolism-
dc.subject.meshReceptors, CCR3 - genetics - immunology - metabolism-
dc.subject.meshReceptors, CCR5 - genetics - immunology - metabolism-
dc.subject.meshSARS Virus - immunology - pathogenicity-
dc.titleToll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://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+cellsen_HK
dc.identifier.emailCheung, CY: chungey@hkucc.hku.hken_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.authorityCheung, CY=rp00404en_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1471-2172-10-35en_HK
dc.identifier.pmid19505311-
dc.identifier.pmcidPMC2700820-
dc.identifier.scopuseid_2-s2.0-67649887153en_HK
dc.identifier.hkuros164803en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67649887153&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue35-
dc.identifier.isiWOS:000267746900001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridCheung, CY=7202061836en_HK
dc.identifier.scopusauthoridSia, SF=8574447900en_HK
dc.identifier.scopusauthoridChan, YO=55065554600en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.citeulike4841273-

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