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- W2959246123 abstract "Summary Inflammasomes and interferons constitute two critical arms of innate immunity. Most facultative bacterial pathogens that inhabit the host cell cytosol avoid activating inflammasomes and are often resistant to killing by type I interferon (IFN-I). We report that the human pathogen Rickettsia parkeri, an obligate intracellular pathogen that resides in the cytosol, is sensitive to IFN-I. The mechanism of IFN-I-dependent restriction requires the transcription factor IRF5, which upregulates anti-rickettsial factors including guanylate-binding proteins and iNOS. However, R. parkeri curtails cGAS-dependent IFN-I production by causing caspase-11-dependent pyroptosis. In vivo , inflammasome activation antagonizes IFN-I production, enhancing R. parkeri abundance in the spleen. Mice lacking either IFN-I or IFN-γ signaling are resistant to infection, but mice lacking both rapidly succumb, revealing that both interferons are required to control R. parkeri . This study illuminates how an obligate cytosolic pathogen exploits the intrinsic trade-off between cell death and cytokine production to escape killing by innate immunity. Highlights Rickettsia killed by GBPs activates caspase-11 and GSDMD, promoting pyroptosis Rickettsia exploits pyroptosis to avoid cGAS-dependent type I interferon IRF5, GBPs, and iNOS contribute to controlling R. parkeri infection Ifnar -/- Ifngr -/- mice succumb to infection, uncovering a mouse model to study R. parkeri" @default.
- W2959246123 created "2019-07-23" @default.
- W2959246123 creator A5002707693 @default.
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- W2959246123 creator A5061473047 @default.
- W2959246123 creator A5085453391 @default.
- W2959246123 date "2019-07-11" @default.
- W2959246123 modified "2023-09-25" @default.
- W2959246123 title "Inflammasome-mediated antagonism of type I interferon enhancesRickettsiapathogenesis" @default.
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- W2959246123 doi "https://doi.org/10.1101/697573" @default.
- W2959246123 hasPublicationYear "2019" @default.
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