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Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases
Cited 1028 time in
Web of Science
Cited 1105 time in Scopus
- Authors
- Issue Date
- 2017-05
- Publisher
- Blackwell Publishing Inc.
- Citation
- Immunological Reviews, Vol.277 No.1, pp.61-75
- Abstract
- Cell death is a fundamental biological phenomenon that is essential for the survival and development of an organism. Emerging evidence also indicates that cell death contributes to immune defense against infectious diseases. Pyroptosis is a form of inflammatory programmed cell death pathway activated by human and mouse caspase-1, human caspase-4 and caspase-5, or mouse caspase-11. These inflammatory caspases are used by the host to control bacterial, viral, fungal, or protozoan pathogens. Pyroptosis requires cleavage and activation of the pore-forming effector protein gasdermin D by inflammatory caspases. Physical rupture of the cell causes release of the pro-inflammatory cytokines IL-1 beta and IL-18, alarmins and endogenous danger-associated molecular patterns, signifying the inflammatory potential of pyroptosis. Here, we describe the central role of inflammatory caspases and pyroptosis in mediating immunity to infection and clearance of pathogens.
- ISSN
- 0105-2896
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