Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 2006 Feb 28;103(9):3363-8.
doi: 10.1073/pnas.0511345103. Epub 2006 Feb 21.

Gene expression patterns in dendritic cells infected with measles virus compared with other pathogens

Michael J Zilliox  1 , Giovanni Parmigiani, Diane E Griffin
Affiliations
Comparative Study

Gene expression patterns in dendritic cells infected with measles virus compared with other pathogens

Michael J Zilliox et al. Proc Natl Acad Sci U S A. .

Abstract

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.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest statement: No conflicts declared.

Figures

Fig. 1.
Fig. 1.
Induction of IFN-α genes. (A) IFN-α gene expression. Time course of IFN-α gene expression for DCs exposed to MV, C. albicans, E. coli, influenza virus, or media. RNAs were collected at various time points, and expression levels were measured by microarray analysis. The lines show the mean fold changes normalized to the preexposure 0 time point, and the points show the actual fold changes. Data for C. albicans, E. coli, and influenza virus are from Huang et al. (15). (B) Production of biologically active IFN by MV-infected DCs. Points show the calculated IFN units per milliliter for the replicates and the line shows the means.
Fig. 2.
Fig. 2.
Induction of IFN-β, IFN-γ, and IFN-ω genes. Time courses of IFN-β, IFN-γ, and IFN-ω for DCs exposed to MV, C. albicans, E. coli, influenza virus, or media. RNA analysis, data sources, and plotting are as described for Fig. 1A.
Fig. 3.
Fig. 3.
Induction of representative chemokine and antiviral protein genes. Time courses for CCL5, CCL20, CCR7, Mx1, and PKR gene expression for DCs exposed to MV, C. albicans, E. coli, influenza virus, or media. RNA analysis, data sources, and plotting are as described for Fig. 1A.
Fig. 4.
Fig. 4.
Induction of representative IL, metallothionein, and TNFSF member genes. Time courses for IL-6, IL-15, MT-1F, TNFSF8, and TNFSF10 for DCs exposed to MV, C. albicans, E. coli, influenza virus, or media. RNA analysis, data sources, and plotting are as described for Fig. 1A.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Stein C. E., Birmingham M., Kurian M., Duclos P., Strebel P. J. Infect. Dis. 2003;187(Suppl. 1):S8–S14. - PubMed
    1. Griffin D. E. Curr. Top. Microbiol. Immunol. 1995;191:117–134. - PubMed
    1. Esolen L. M., Ward B. J., Moench T. R., Griffin D. E. J. Infect. Dis. 1993;168:47–52. - PubMed
    1. Moench T. R., Griffin D. E., Obriecht C. R., Vaisberg A. J., Johnson R. T. J. Infect. Dis. 1988;158:433–442. - PubMed
    1. Schneider-Schaulies S., Bieback K., Avota E., Klagge I., ter Meulen V. J. Mol. Med. 2002;80:73–85. - PubMed

Publication types

MeSH terms

Associated data