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Immunol Rev. 2017 May;277(1):61-75. doi: 10.1111/imr.12534.

Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases.

Author information

1
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.

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-1β 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.

KEYWORDS:

bacteria; caspase-1; caspase-11; caspase-4; caspase-5; cell death; gasdermin D; infection; inflammasomes; inflammation; inflammatory caspases; interferons; lysis; lytic; necroptosis; necrosis; pores; pyroptosis; viruses

PMID:
28462526
PMCID:
PMC5416822
DOI:
10.1111/imr.12534
[Indexed for MEDLINE]
Free PMC Article

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