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Type I IFN Responses (type + i_ifn_response)
Selected AbstractsBreastfeeding is associated with the production of type I interferon in infants infected with influenza virusACTA PAEDIATRICA, Issue 10 2010Guillermina A Melendi Abstract Background:, Breast milk-mediated protection against respiratory viruses is well established. However, protective mechanisms are unclear. Type I interferons (IFN) mediate host defence against respiratory viruses, particularly influenza virus. The relationship among type I IFN, respiratory viral infections and breastfeeding has not been explored. Methods:, Type I IFN responses were studied by ELISA and real time PCR in nasal secretions of infants experiencing their first respiratory infection. Modulation of IFN by breastfeeding and other variables affecting severity during viral infection was explored. Results:, One hundred and twenty infants were positive by RT-PCR for influenza virus (n = 24), human metapneumovirus (hMPV) (n = 30) or respiratory syncytial virus (RSV) (n = 66). Type I IFNs were detected more frequently in infants infected with influenza virus than in those infected with RSV or hMPV. Breastfeeding promoted higher rates and levels of type I IFN only in infants infected with influenza virus. No effect on IFN production was observed for age, gender or smoking. Conclusion:, Our study confirms that type I IFN production is detected more frequently in infants infected with influenza virus. Importantly, higher rates and levels of type I IFN in these infants are associated with breastfeeding. These observations suggest that breast milk can protect against respiratory viruses by activating innate antiviral mechanisms in the host. [source] The IFN regulatory factor 7-dependent type I IFN response is not essential for early resistance against murine cytomegalovirus infectionEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2009Christian Steinberg 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-, response to MCMV was entirely dependent on IRF7, but independent of IRF3. However, peak IFN-, production during MCMV infection was not affected by the lack of IRF7 or both IRF7 and IRF3. Despite the complete lack of IFN-, 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-, 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. [source] TLR pathways and IFN-regulatory factors: To each its ownEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 2 2007Marco Colonna Abstract TLR trigger the induction of type I IFN (IFN-alpha/beta), providing a crucial mechanism of anti-viral defense. Until recently, TLR were thought to induce type I IFN responses by activating two transcription factors which belong to the IFN-regulatory factor (IRF) family, IRF-3 and IRF-7. TLR-3 and TLR-4 induce IFN-beta by activating IRF-3; TLR-9 induces IFN-alpha and IFN-beta through IRF-7, at least when engaged by type A CpG oligonucleotides (CpG-A) in plasmacytoid DC (pDC). In this issue of the European Journal of Immunology, it is demonstrated that TLR-9 induces IFN-beta when engaged by type B CpG oligonucleotides (CpG-B) in myeloid DC and macrophages. Remarkably, this response is independent of IRF-3/7 and, in fact, requires another IRF family member, IRF-1. IRF-1 is recruited by TLR-9 through the adaptor MyD88. Deficiency of the TLR-9,IRF-1,IFN-beta pathway results in impaired anti-viral responses not only in vitro but also in vivo. These results demonstrate that TLR induce IFN-alpha or IFN-beta responses by activating distinct IRF, depending on the TLR ligand and the cell type. These distinct TLR-IRF pathways may allow the immune system to tailor its responses to viral pathogens. See accompanying article http://dx.doi.org/10.1002/eji.200636767 [source] | ||||||||||