Abstract
Inflammasomes are macromolecular complexes formed in response to pathogen‐associated molecular patterns (PAMPs) and danger‐associated molecular patterns (DAMPs) that drive maturation of the pro‐inflammatory cytokines interleukin (IL)‐1β and IL‐18, and cleave gasdermin D (GSDMD) for induction of pyroptosis. Inflammasomes are highly important in protecting the host from various microbial pathogens and sterile insults. Inflammasome pathways are strictly regulated at both transcriptional and post‐translational checkpoints. When these checkpoints are not properly imposed, undue inflammasome activation may promote inflammatory, metabolic and oncogenic processes that give rise to autoinflammatory, autoimmune, metabolic and malignant diseases. In addition to clinically approved IL‐1‐targeted biologics, upstream targeting of inflammasome pathways recently gained interest as a novel pharmacological strategy for selectively modulating inflammasome activation in pathological conditions.
Highlights
Our innate immune system orchestrates a first and rapid response against microbial pathogens and sterile damage
These results raise the possibility that MCC950/CRID3-based therapies may need to be dosed at higher concentrations in Cryopyrin-Associated Periodic Syndrome (CAPS) patients to effectively treat inflammatory pathology than is needed to curb inflammatory pathology driven by wildtype NLRP3
Results from Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) suggest that canakinumab-mediated blockage of IL-1β activity protects against the development of lung cancer, the mechanism involved remains unclear
Summary
Our innate immune system orchestrates a first and rapid response against microbial pathogens and sterile damage.
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