2017/04/30 by Si Ming Man, Rajendra Karki, Thirumala‐Devi Kanneganti · 4 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #Autoimmune and Inflammatory Disorders Research #Inflammasome and immune disorders #Kawasaki Disease and Coronary Complications
paper · doi:10.1111/imr.12534
openalex publication_date 2017/04/30 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/25
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.