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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Virus-induced interferon alpha production by a dendritic cell subset in the absence of feedback signaling in vivo.

An effective type I interferon (IFN-alpha/beta) 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-alpha is dependent on type I IFN receptor (IFNAR) triggering, whereas in infected mice early IFN-alpha 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((R))-sorted CD11c(int)CD11b(-)GR-1(+) DCs show high IFN-alpha 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-alpha largely independent of IFNAR feedback signaling.[1]

References

  1. Virus-induced interferon alpha production by a dendritic cell subset in the absence of feedback signaling in vivo. Barchet, W., Cella, M., Odermatt, B., Asselin-Paturel, C., Colonna, M., Kalinke, U. J. Exp. Med. (2002) [Pubmed]
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