Journal
NATURE REVIEWS MICROBIOLOGY
Volume 7, Issue 2, Pages 99-109Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrmicro2070
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Funding
- National Institutes of Health [AI47242, P50 HG02360]
- Poncin and Achievement Rewards for College Scientist Fellowships
- National Institute of General Medical Sciences Public Health Service National Research Service Award [T32 GM07270]
- Helen Riaboff Whitely Fellowship
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Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
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