title: Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Paediatrics and Adolescent Medicine, Hong Kong Jockey Club Clinical Research Centre, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong, PR China. hkwlaw@hkucc.hku.hk
authors.forename: Helen K W
authors.initials: HK
authors.lastname: Law
authors.forename: Chung Yan
authors.initials: CY
authors.lastname: Cheung
authors.forename: Sin Fun
authors.initials: SF
authors.lastname: Sia
authors.forename: Yuk On
authors.initials: YO
authors.lastname: Chan
authors.forename: J S Malik
authors.initials: JS
authors.lastname: Peiris
authors.forename: Yu Lung
authors.initials: YL
authors.lastname: Lau
mesh_terms: D000328:Adult; D000367:Age Factors; D002478:Cells, Cultured; D002681:China; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D053222:Fas Ligand Protein / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D005260:Female; D005312:Fetal Blood; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D009000:Monocytes / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D054389:Receptors, CCR1 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D054397:Receptors, CCR3 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D019713:Receptors, CCR5 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D045473:Severe acute respiratory syndrome-related coronavirus / Q000276:immunology* / Q000472:pathogenicity; D045169:Severe Acute Respiratory Syndrome / Q000097:blood / Q000453:epidemiology / Q000276:immunology* / Q000503:physiopathology; D012720:Severity of Illness Index; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D051194:Toll-Like Receptor 1 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D051201:Toll-Like Receptor 10 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D014774:Virulence / Q000276:immunology
chemical_list: D053222:Fas Ligand Protein; D054389:Receptors, CCR1; D054397:Receptors, CCR3; D019713:Receptors, CCR5; D053221:TNF-Related Apoptosis-Inducing Ligand; D051194:Toll-Like Receptor 1; D051201:Toll-Like Receptor 10