Format

Send to

Choose Destination
Eur J Immunol. 2009 Apr;39(4):1007-18. doi: 10.1002/eji.200838814.

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

Author information

1
II. Medizinische Klinik, Klinikum Rechts der Isar, Technical University Munich, Munich, Germany.

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-alpha response to MCMV was entirely dependent on IRF7, but independent of IRF3. However, peak IFN-beta production during MCMV infection was not affected by the lack of IRF7 or both IRF7 and IRF3. Despite the complete lack of IFN-alpha 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-gamma 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.

PMID:
19283778
DOI:
10.1002/eji.200838814
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center