An effective type I interferon (IFN-α/β) 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-α is dependent on type I IFN receptor (IFNAR) triggering, whereas in infected mice early IFN-α 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-α largely independent of IFNAR feedback signaling.

Original languageEnglish
Pages (from-to)507-516
Number of pages10
JournalJournal of Experimental Medicine
Issue number4
StatePublished - Feb 18 2002


  • Dendritic cell subsets
  • IFN regulatory factor 7
  • IFN type I
  • Type I IFN receptor
  • Virus infection


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