The IFN regulatory factor 7-dependent type I IFN response is not essential for early resistance against murine cytomegalovirus infection

Christrian Steinberg, Katharina Eisenächer, Olaf Gross, Wolfgang Reindl, Frank Schmitz, Jürgen Ruland, Anne Krug

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

IFN regulatory factor 7 (IRF7) has been described as the master regulator of type I IFN responses and has been shown to be critical for innate antiviral immunity in vivo. In addition to type I IFN, NK cell responses are involved in the control of viral replication during acute viral infection. To investigate the role of IRF7 in the context of a viral infection that induces a strong NK cell response, the murine cytomegalovirus (MCMV) infection model was used. WT, IRF7-deficient and IRF3/IRF7-double deficient mice were infected with MCMV. The systemic IFN-α response to MCMV was entirely dependent on IRF7, but independent of IRF3. However, peak IFN-β production during MCMV infection was not affected by the lack of IRF7 or both IRF7 and IRF3. Despite the complete lack of IFN-α production IRF7- and IRF3/ IRF7-deficient mice were surprisingly efficient in controlling MCMV replication and were only modestly more susceptible to MCMV infection than WT mice. NK cell cytotoxicity was unimpaired and NK cell IFN-γ production was enhanced in IRF7-deficient mice correlating with increased levels of bioactive IL-12. Owing to these compensatory mechanisms IRF7-dependent antiviral immune responses were not essential for resistance against acute MCMV infection in vivo.

Original languageEnglish
Pages (from-to)1007-1018
Number of pages12
JournalEuropean Journal of Immunology
Volume39
Issue number4
DOIs
StatePublished - 2009
Externally publishedYes

Keywords

  • IFN regulatory factor
  • Murine cytomegalovirus
  • NK cells
  • Type I IFN

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