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

Si Ming Man, Rajendra Karki, Thirumala Devi Kanneganti*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

1142 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)61-75
Number of pages15
JournalImmunological Reviews
Volume277
Issue number1
DOIs
Publication statusPublished - May 2017
Externally publishedYes

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