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Pyroptotic cell death defends against intracellular pathogens |
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| Authors: | Ine Jorgensen Edward A Miao |
| Institution: | 1. Department of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA;2. Department of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Correspondence to: Edward A. Miao Department of Microbiology and Immunology University of North Carolina at Chapel Hill 125 Mason Farm Road 6th Floor Marsico Hall Chapel Hill, NC 27599-7290, USA Tel.: +1 919 966 6773 e-mail: edward_miao@med.unc.edu |
| Abstract: | Inflammatory caspases play a central role in innate immunity by responding to cytosolic signals and initiating a twofold response. First, caspase-1 induces the activation and secretion of the two prominent pro-inflammatory cytokines, interleukin-1β (IL-1β) and IL-18. Second, either caspase-1 or caspase-11 can trigger a form of lytic, programmed cell death called pyroptosis. Pyroptosis operates to remove the replication niche of intracellular pathogens, making them susceptible to phagocytosis and killing by a secondary phagocyte. However, aberrant, systemic activation of pyroptosis in vivo may contribute to sepsis. Emphasizing the efficiency of inflammasome detection of microbial infections, many pathogens have evolved to avoid or subvert pyroptosis. This review focuses on molecular and morphological characteristics of pyroptosis and the individual inflammasomes and their contribution to defense against infection in mice and humans. |
| Keywords: | caspase-1 caspase-11 inflammasome pyroptosis inflammatory caspases |