Abstract
NLRP3 has a pivotal role in nucleating the inflammasome, a cytoplasmic multiprotein complex that mediates the maturation of the proinflammatory cytokine interleukin-1β (IL-1β) by activating caspase-1. Mutations in the gene encoding NLRP3 cause a spectrum of autoinflammatory disease, the cryopyrin-associated periodic syndromes (CAPS). It has been reported that generation of reactive oxygen species (ROS) is a major NLRP3 inflammasome-activating factor. However, the molecular mechanism by which a change in cellular redox state leads to NLRP3 inflammasome activation has not been elucidated. Here we show that cofilin-1, a redox sensitive actin binding protein, is involved in NLRP3 inflammasome activation.
Highlights
NLRP3 has a pivotal role in nucleating the inflammasome, a cytoplasmic multiprotein complex that mediates the maturation of the proinflammatory cytokine interleukin1b (IL-1b) by activating caspase-1
Mutations in the gene encoding NLRP3 cause a spectrum of autoinflammatory disease, the cryopyrin-associated periodic syndromes (CAPS)
It has been reported that generation of reactive oxygen species (ROS) is a major NLRP3 inflammasomeactivating factor
Summary
NLRP3 has a pivotal role in nucleating the inflammasome, a cytoplasmic multiprotein complex that mediates the maturation of the proinflammatory cytokine interleukin1b (IL-1b) by activating caspase-1. Mutations in the gene encoding NLRP3 cause a spectrum of autoinflammatory disease, the cryopyrin-associated periodic syndromes (CAPS). It has been reported that generation of reactive oxygen species (ROS) is a major NLRP3 inflammasomeactivating factor. The molecular mechanism by which a change in cellular redox state leads to NLRP3 inflammasome activation has not been elucidated. We show that cofilin-1, a redox sensitive actin binding protein, is involved in NLRP3 inflammasome activation
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