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Original Article

Virus-induced Interferon Production by a Dendritic Cell Subset in the Absence of Feedback Signaling In Vivo

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 CD11c^intCD11b^-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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