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Journal of Virology, July 2007, p. 7749-7758, Vol. 81, No. 14
0022-538X/07/$08.00+0     doi:10.1128/JVI.02438-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Type III Interferon (IFN) Induces a Type I IFN-Like Response in a Restricted Subset of Cells through Signaling Pathways Involving both the Jak-STAT Pathway and the Mitogen-Activated Protein Kinases{triangledown} ,{dagger}

Zhangle Zhou,1,{ddagger} Ole J. Hamming,2,{ddagger} Nina Ank,3 Søren R. Paludan,3 Anders L. Nielsen,1 and Rune Hartmann2*

Department of Human Genetics, University of Aarhus, Denmark,1 Centre for Structural Biology, Department of Molecular Biology, University of Aarhus, Denmark,2 Institute of Medical Microbiology and Immunology, University of Aarhus, Denmark3

Received 6 November 2006/ Accepted 4 May 2007

Type III interferon (IFN) is a novel member of the interferon family. Type III IFN utilizes a receptor complex different from that of type I IFN, but both types of IFN induce STAT1, STAT2, and STAT3 activation. Here we describe a detailed comparison of signal transduction initiated by type I and type III IFN. Gene expression array analysis showed that IFN types I and III induced a similar subset of genes. In particular, no genes were induced uniquely by type III IFN. Next, we used chromatin immunoprecipitation (ChIP) analysis to investigate the promoter activation by types I and III IFN. The ChIP assays demonstrated that stimulation of cells with both type I and type III IFN resulted in the recruitment of ISGF3 transcription factor components to the promoter region of responsive genes and in an increase of polymerase II loading and histone acetylation. Whereas IFN type I signaling was observed for a broad spectrum of cell lines, type III IFN signaling was more restricted. The lack of IFN type III signaling was correlated with a low expression of the IL28Ra component of the IFN type III receptor, and IL28Ra overexpression was sufficient to restore IFN type III signaling. We also tested the activation of mitogen-activated protein (MAP) kinases by type III IFN and found that type III IFN relies strongly upon both p38 and JNK MAP kinases for gene induction.

* Corresponding author. Mailing address: Department of Molecular Biology, Gustav Wieds vej 10C, 8000 Århus C, Denmark. Phone: 45 89425279. Fax: 45 86123178. E-mail: rh{at}mb.au.dk

{triangledown} Published ahead of print on 16 May 2007.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} These authors contributed equally to this work.

Journal of Virology, July 2007, p. 7749-7758, Vol. 81, No. 14
0022-538X/07/$08.00+0     doi:10.1128/JVI.02438-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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