Published 19 February 2002. doi:10.1084/jem.20011666
© Rockefeller University Press, 0022-1007/2002/2/507/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 4, February 18, 2002 507-516
Virus-induced Interferon
Production by a Dendritic Cell Subset in the Absence of Feedback Signaling In Vivo
Winfried Barchet1,
Marina Cella2,
Bernhard Odermatt3,
Carine Asselin-Paturel4,
Marco Colonna2 and
Ulrich Kalinke1
1 Mouse Biology Programme, EMBL-Monterotondo, I-00016 Monterotondo-Scalo (Roma), Italy
2 Basel Institute for Immunology, CH-4005 Basel, Switzerland
3 Department of Pathology, University of Zürich, CH-8091 Zürich, Switzerland
4 Schering-Plough, Laboratory for Immunological Research, Dardilly T-69570, France
Address correspondence to Ulrich Kalinke, Dept. of Immunology, Paul-Ehrlich-Institute, Paul-Ehrlich-Str. 51-59, D-3225 Langen, Germany. Phone: 49-6103-77-2002/3; Fax: 49-6103-77-1253; E-mail: kalul{at}pei.de
An effective type I interferon (IFN-
/ß) response is critical for the control of many viral infections. Here we show that in vesicular stomatitis virus (VSV)-infected mouse embryonic fibroblasts (MEFs) the production of IFN-
is dependent on type I IFN receptor (IFNAR) triggering, whereas in infected mice early IFN-
production is IFNAR independent. In VSV-infected mice type I IFN is produced by few cells located in the marginal zone of the spleen. Unlike other dendritic cell (DC) subsets, FACS®-sorted CD11cintCD11b-GR-1+ DCs show high IFN-
expression, irrespective of whether they were isolated from VSV-infected IFNAR-competent or -deficient mice. Thus, VSV preferentially activates a specialized DC subset presumably located in the marginal zone to produce high-level IFN-
largely independent of IFNAR feedback signaling.
Key Words: IFN type I virus infection dendritic cell subsets IFN regulatory factor 7 type I IFN receptor

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