PMID- 16492729
OWN - NLM
STAT- MEDLINE
DCOM- 20060410
LR  - 20240322
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 103
IP  - 9
DP  - 2006 Feb 28
TI  - Gene expression patterns in dendritic cells infected with measles virus compared 
      with other pathogens.
PG  - 3363-8
AB  - Gene expression patterns supply insight into complex biological networks that 
      provide the organization in which viruses and host cells interact. Measles virus 
      (MV) is an important human pathogen that induces transient immunosuppression 
      followed by life-long immunity in infected individuals. Dendritic cells (DCs) are 
      potent antigen-presenting cells that initiate the immune response to pathogens 
      and are postulated to play a role in MV-induced immunosuppression. To better 
      understand the interaction of MV with DCs, we examined the gene expression 
      changes that occur over the first 24 h after infection and compared these changes 
      to those induced by other viral, bacterial, and fungal pathogens. There were 
      1,553 significantly regulated genes with nearly 60% of them down-regulated. 
      MV-infected DCs up-regulated a core of genes associated with maturation of 
      antigen-presenting function and migration to lymph nodes but also included genes 
      for IFN-regulatory factors 1 and 7, 2'5' oligoadenylate synthetase, Mx, and TNF 
      superfamily proteins 2, 7, 9, and 10 (TNF-related apoptosis-inducing ligand). MV 
      induced genes for IFNs, ILs, chemokines, antiviral proteins, histones, and 
      metallothioneins, many of which were also induced by influenza virus, whereas 
      genes for protein synthesis and oxidative phosphorylation were down-regulated. 
      Unique to MV were the induction of genes for a broad array of IFN-alphas and the 
      failure to up-regulate dsRNA-dependent protein kinase. These results provide a 
      modular view of common and unique DC responses after infection and suggest 
      mechanisms by which MV may modulate the immune response.
FAU - Zilliox, Michael J
AU  - Zilliox MJ
AD  - The W. Harry Feinstone Department of Molecular Microbiology and Immunology, The 
      Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
FAU - Parmigiani, Giovanni
AU  - Parmigiani G
FAU - Griffin, Diane E
AU  - Griffin DE
LA  - eng
SI  - OMIM/GSE980
GR  - R01 AI023047/AI/NIAID NIH HHS/United States
GR  - T32 ES007141/ES/NIEHS NIH HHS/United States
GR  - T32 ES07141/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20060221
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Chemokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9008-11-1 (Interferons)
RN  - 9038-94-2 (Metallothionein)
SB  - IM
MH  - Animals
MH  - Bacteria/*immunology
MH  - Cells, Cultured
MH  - Chemokines/genetics
MH  - Chlorocebus aethiops
MH  - Dendritic Cells/*metabolism/microbiology/*virology
MH  - Down-Regulation/genetics
MH  - Fungi/immunology/*physiology
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Interferons/genetics
MH  - Measles virus/immunology/*physiology
MH  - Metallothionein/genetics
MH  - Tumor Necrosis Factor-alpha/classification/genetics
MH  - Up-Regulation/genetics
PMC - PMC1413941
COIS- Conflict of interest statement: No conflicts declared.
EDAT- 2006/02/24 09:00
MHDA- 2006/04/11 09:00
PMCR- 2006/08/28
CRDT- 2006/02/24 09:00
PHST- 2006/02/24 09:00 [pubmed]
PHST- 2006/04/11 09:00 [medline]
PHST- 2006/02/24 09:00 [entrez]
PHST- 2006/08/28 00:00 [pmc-release]
AID - 0511345103 [pii]
AID - 1308 [pii]
AID - 10.1073/pnas.0511345103 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3363-8. doi: 
      10.1073/pnas.0511345103. Epub 2006 Feb 21.