Abstract
Mutations in the gene encoding NLRP3 cause a spectrum of autoinflammatory diseases known as the cryopyrin-associated periodic syndromes (CAPS). NLRP3 is a key component of one of several distinct cytoplasmic multiprotein complexes (inflammasomes) that mediate the maturation of the proinflammatory cytokine interleukin-1β (IL-1β) by activating caspase-1. Although several models for inflammasome activation, such as K+ efflux, generation of reactive oxygen species, and lysosomal destabilization have been proposed, the precise molecular mechanism of NLRP3 inflammasome activation, as well as the mechanism by which CAPS-associated mutations activate NLRP3, remains to be elucidated.
Highlights
Mutations in the gene encoding NLRP3 cause a spectrum of autoinflammatory diseases known as the cryopyrinassociated periodic syndromes (CAPS)
NLRP3 is a key component of one of several distinct cytoplasmic multiprotein complexes that mediate the maturation of the proinflammatory cytokine interleukin1b (IL-1b) by activating caspase-1
Using a combination of genetic, pharmacological, and biochemical approaches, we provide evidence that the CaSR is essential for NLRP3 inflammasome activation, which is directly controlled by intracellular Ca2+ and cAMP
Summary
OR11-003 - The NLRP3 inflammasome is regulated by CaSR Introduction Mutations in the gene encoding NLRP3 cause a spectrum of autoinflammatory diseases known as the cryopyrinassociated periodic syndromes (CAPS). NLRP3 is a key component of one of several distinct cytoplasmic multiprotein complexes (inflammasomes) that mediate the maturation of the proinflammatory cytokine interleukin1b (IL-1b) by activating caspase-1.
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