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nature portfolio permissions reprints privacy policy advertising national research council obtained research funding receptor-interacting kinase-3-mediated pathway nature 430 nature 471 nature cytomegalovirus rip1-interacting protein social media health research cancer research hiv-infected adults author correspondence smac mimetics-induced apoptosis ity/lsh/bcg locus phosphoinositide 3-kinase/mammalian target cross-journal web focus l929-isre cell line salmonella typhimurium-mediated injury interferon α-induced apoptosis typhimurium–induced cell death rip3-dependent necrosis springerlink instant access caspase-1-dependent necrosis permissions development salmonella exploits caspase-1 personal data kinase rip3 prevented apoptosis proteins ciap1 salmonella typhimurium strains salmonella typhimurium pathogenesis salmonella typhimurium leading salmonella typhimurium infection cellular stress responses data protection virulent salmonella typhimurium tnf-induced necrosis murine typhoid model privacy specific cellular target bacterial virulence determinants prolonged antigen presentation competing financial interests molecular signaling network caspase-1-mediated activation host immune responses

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• Type I interferon signaling and macrophages: a double-edged sword?

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         description:The role of type I interferon in bacterial infection is poorly understood. Sad and colleagues demonstrate that Salmonella-triggered production of type I interferon induces macrophage necroptosis, evasion of the immune response and dissemination of bacteria. Salmonella enterica serovar Typhimurium (S. Typhimurium) is a virulent pathogen that induces rapid host death. Here we observed that host survival after infection with S. Typhimurium was enhanced in the absence of type I interferon signaling, with improved survival of mice deficient in the receptor for type I interferons (Ifnar1−/− mice) that was attributed to macrophages. Although there was no impairment in cytokine expression or inflammasome activation in Ifnar1−/− macrophages, they were highly resistant to S. Typhimurium–induced cell death. Specific inhibition of the kinase RIP1 or knockdown of the gene encoding the kinase RIP3 prevented the death of wild-type macrophages, which indicated that necroptosis was a mechanism of cell death. Finally, RIP3-deficient macrophages, which cannot undergo necroptosis, had similarly less death and enhanced control of S. Typhimurium in vivo. Thus, we propose that S. Typhimurium induces the production of type I interferon, which drives necroptosis of macrophages and allows them to evade the immune response.
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      name:National Research Council of Canada–Institute for Biological Sciences, Ottawa, Canada
      name:Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Canada
      name:National Research Council of Canada–Institute for Biological Sciences, Ottawa, Canada
      name:Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Canada
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