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Journal of Virology, August 2005, p. 9608-9617, Vol. 79, No. 15
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.15.9608-9617.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Gene Expression and Antiviral Activity of Alpha/Beta Interferons and Interleukin-29 in Virus-Infected Human Myeloid Dendritic Cells

Pamela Österlund,1 Ville Veckman,1 Jukka Sirén,1 Kevin M. Klucher,2 John Hiscott,3 Sampsa Matikainen,1 and Ilkka Julkunen1*

Department of Viral Diseases and Immunology, National Public Health Institute, FIN-00300 Helsinki, Finland,1 ZymoGenetics, Inc., Eastlake Ave. E., Seattle, Washington 98102,2 Lady Davis Institute for Medical Research and Departments of Microbiology and Immunology & Medicine, McGill University, Montreal, Quebec, Canada H3T 1E23

Received 5 January 2005/ Accepted 19 April 2005

Dendritic cells (DCs) respond to microbial infections by undergoing phenotypic maturation and by producing multiple cytokines. In the present study, we analyzed the ability of influenza A and Sendai viruses to induce DC maturation and activate tumor necrosis factor alpha (TNF-{alpha}), alpha/beta interferon (IFN-{alpha}/ß), and IFN-like interleukin-28A/B (IFN-{lambda}2/3) and IL-29 (IFN-{lambda}1) gene expression in human monocyte-derived myeloid DCs (mDC). The ability of influenza A virus to induce mDC maturation or enhance the expression of TNF-{alpha}, IFN-{alpha}/ß, interleukin-28 (IL-28), and IL-29 genes was limited, whereas Sendai virus efficiently induced mDC maturation and enhanced cytokine gene expression. Influenza A virus-induced expression of TNF-{alpha}, IFN-{alpha}, IFN-ß, IL-28, and IL-29 genes was, however, dramatically enhanced when cells were pretreated with IFN-{alpha}. IFN-{alpha} priming led to increased expression of Toll-like receptor 3 (TLR3), TLR7, TLR8, MyD88, TRIF, and IFN regulatory factor 7 (IRF7) genes and enhanced influenza-induced phosphorylation and DNA binding of IRF3. Influenza A virus also enhanced the binding of NF-{kappa}B to the respective NF-{kappa}B elements of the promoters of IFN-ß and IL-29 genes. In mDC IL-29 induced MxA protein expression and possessed antiviral activity against influenza A virus, although this activity was lower than that of IFN-{alpha} or IFN-ß. Our results show that in human mDCs viruses can readily induce the expression of IL-28 and IL-29 genes whose gene products are likely to contribute to the host antiviral response.

* Corresponding author. Mailing address: Department of Viral Diseases and Immunology, National Public Health Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland. Phone: 358-9-47448372. Fax: 358-9-47448355. E-mail: ilkka.julkunen{at}ktl.fi.

Journal of Virology, August 2005, p. 9608-9617, Vol. 79, No. 15
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.15.9608-9617.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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