PMID- 17913823
OWN - NLM
STAT- MEDLINE
DCOM- 20071227
LR  - 20211020
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 81
IP  - 24
DP  - 2007 Dec
TI  - Differential activation of human monocyte-derived and plasmacytoid dendritic 
      cells by West Nile virus generated in different host cells.
PG  - 13640-8
AB  - Dendritic cells (DCs) play a central role in innate immunity and antiviral 
      responses. In this study, we investigated the production of alpha interferon 
      (IFN-alpha) and inducible chemokines by human monocyte-derived dendritic cells 
      (mDCs) and plasmacytoid dendritic cells (pDCs) infected with West Nile virus 
      (WNV), an emergent pathogen whose infection can lead to severe cases of 
      encephalitis in the elderly, children, and immunocompromised individuals. Our 
      experiments demonstrated that WNV grown in mammalian cells (WNV(Vero)) was a 
      potent inducer of IFN-alpha secretion in pDCs and, to a lesser degree, in mDCs. 
      The ability of WNV(Vero) to induce IFN-alpha in pDCs did not require viral 
      replication and was prevented by the treatment of cells with bafilomycin A1 and 
      chloroquine, suggesting that it was dependent on endosomal Toll-like receptor 
      recognition. On the other hand, IFN-alpha production in mDCs required viral 
      replication and was associated with the nuclear translocation of IRF3 and viral 
      antigen expression. Strikingly, pDCs failed to produce IFN-alpha when stimulated 
      with WNV grown in mosquito cells (WNV(C7/10)), while mDCs responded similarly to 
      WNV(Vero) or WNV(C7/10). Moreover, the IFN-dependent chemokine IP-10 was produced 
      in substantial amounts by pDCs in response to WNV(Vero) but not WNV(C7/10), while 
      interleukin-8 was produced in greater amounts by mDCs infected with WNV(C7/10) 
      than in those infected with WNV(Vero). These findings suggest that cell-specific 
      mechanisms of WNV recognition leading to the production of type I IFN and 
      inflammatory chemokines by DCs may contribute to both the innate immune response 
      and disease pathogenesis in human infections.
FAU - Silva, Maria Carlan
AU  - Silva MC
AD  - Department of Pathology, 3.206B Mary Moody Northen Pavilion, University of Texas 
      Medical Branch, 301 University Boulevard, Galveston, TX 77555-0436, USA.
FAU - Guerrero-Plata, Antonieta
AU  - Guerrero-Plata A
FAU - Gilfoy, Felicia D
AU  - Gilfoy FD
FAU - Garofalo, Roberto P
AU  - Garofalo RP
FAU - Mason, Peter W
AU  - Mason PW
LA  - eng
GR  - P01 AI062885/AI/NIAID NIH HHS/United States
GR  - AI07526/AI/NIAID NIH HHS/United States
GR  - T32 AI007526/AI/NIAID NIH HHS/United States
GR  - U01 AI061441/AI/NIAID NIH HHS/United States
GR  - AI061441/AI/NIAID NIH HHS/United States
GR  - U54 AI057156/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20071003
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Chemokines)
RN  - 0 (Interferon-alpha)
SB  - IM
MH  - Aedes/virology
MH  - Animals
MH  - Cell Differentiation
MH  - Cell Line
MH  - Cells, Cultured
MH  - Chemokines/*metabolism
MH  - Chlorocebus aethiops
MH  - Dendritic Cells/classification/*cytology/*virology
MH  - Humans
MH  - Interferon-alpha/*metabolism
MH  - Monocytes/cytology/*virology
MH  - Species Specificity
MH  - Vero Cells
MH  - Virus Replication
MH  - West Nile virus/*pathogenicity/physiology
PMC - PMC2168853
EDAT- 2007/10/05 09:00
MHDA- 2007/12/28 09:00
PMCR- 2008/04/01
CRDT- 2007/10/05 09:00
PHST- 2007/10/05 09:00 [pubmed]
PHST- 2007/12/28 09:00 [medline]
PHST- 2007/10/05 09:00 [entrez]
PHST- 2008/04/01 00:00 [pmc-release]
AID - JVI.00857-07 [pii]
AID - 0857-07 [pii]
AID - 10.1128/JVI.00857-07 [doi]
PST - ppublish
SO  - J Virol. 2007 Dec;81(24):13640-8. doi: 10.1128/JVI.00857-07. Epub 2007 Oct 3.