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- W4313383786 abstract "Abstract The innate immune system is essential for detection and elimination of pathogenic microbes. Francisella is an intracellular pathogen that replicates in the cytosol of macrophages. In the cytosol, it can be recognized by host defense sensors. Francisella is sensed by cyclic GMP-AMP synthase (c-GAS) leading to the production of type I Interferons (IFN). It can also be recognized by the PYHIN DNA sensor absent in melanoma (AIM2) resulting in the activation of inflammasome responses i.e. production of pro-inflammatory cytokines IL-1b and IL-18 as well as pyroptosis. While mice deficient in inflammasome components are more susceptible to Francisella infection, type I interferon signaling deficient mice are resistant to Francisella bacterial infection. Inflammasome activation results in gasdermin-D cleavage leading to pyroptotic cell death. Our results show that gasdermin-D activation plays an important role in the nature of cytokine responses to Francisella infection, therefore influencing the outcome of the infection. These findings have major implications in understanding the balance of cytokine production in response to cytosolic immune surveillance." @default.
- W4313383786 created "2023-01-06" @default.
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- W4313383786 date "2018-05-01" @default.
- W4313383786 modified "2023-09-23" @default.
- W4313383786 title "Gasdermin-D controls cytokine responses in <i>Francisella</i> infection." @default.
- W4313383786 doi "https://doi.org/10.4049/jimmunol.200.supp.115.14" @default.
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