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- W2952076359 abstract "Summary Protection from infectious disease relies on two distinct mechanisms. “Antimicrobial resistance” directly inhibits pathogen growth, whereas “infection tolerance” controls tissue damage. A single immune-mediator can differentially contribute to these mechanisms in distinct contexts, confounding our understanding of protection to different pathogens. For example, the NADPH-dependent phagocyte oxidase complex (Phox) produces anti-microbial superoxides and protects from tuberculosis in humans. However, Phox-deficient mice do not display the expected defect in resistance to M. tuberculosis leaving the role of this complex unclear. We re-examined the mechanisms by which Phox contributes to protection from TB and found that mice lacking the Cybb subunit of Phox suffered from a specific defect in tolerance, which was due to unregulated Caspase1 activation, IL-1β production, and neutrophil influx into the lung. These studies demonstrate that Phox-derived superoxide protect against TB by promoting tolerance to persistent infection, and highlight a central role for Caspase1 in regulating TB disease progression." @default.
- W2952076359 created "2019-06-27" @default.
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- W2952076359 date "2017-12-21" @default.
- W2952076359 modified "2023-10-03" @default.
- W2952076359 title "The Phagocyte Oxidase Controls Tolerance toMycobacterium tuberculosisinfection" @default.
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- W2952076359 doi "https://doi.org/10.1101/232777" @default.
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