Journal
YEAR IN IMMUNOLOGY: MYELOID CELLS AND INFLAMMATION
Volume 1319, Issue -, Pages 82-95Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12458
Keywords
NLRP3; inflammasome; caspase-1; mitochondria; calcium
Categories
Funding
- NIH [R01 AI087630, R01 AI104706, T32 AI007511]
- Asthma and Allergy Foundation of America
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI087630, T32AI007511, R01AI104706] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES005605] Funding Source: NIH RePORTER
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Inflammasomes continue to generate interest in an increasing number of disciplines owing to their unique ability to integrate a myriad of signals from pathogen-and damage-associated molecular patterns into a proinflammatory response. This potent caspase-1-dependent process is capable of activating the innate immune system, initiating pyroptosis (an inflammatory form of programmed cell death), and shaping adaptive immunity. The NLRP3 inflammasome is the most thoroughly studied of the inflammasome complexes that have been described thus far, perhaps owing to its disparate assortment of agonists. This review highlights our current understanding of the mechanisms of both priming and activation of the NLRP3 inflammasome.
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