The study investigates the role of cryopyrin (Nalp3) in the activation of caspase-1 and the production of inflammatory cytokines IL-1β and IL-18. Cryopyrin deficiency in mice results in the inability to activate caspase-1 and produce IL-1β and IL-18 in response to bacterial RNA and synthetic compounds R837 and R848. However, other inflammatory cytokines such as TNF-α and IL-6, as well as the activation of NF-κB and MAPKs, are unaffected. The study also shows that Toll-like receptors (TLRs) and cryopyrin control the secretion of IL-1β and IL-18 through different intracellular pathways. These findings highlight the critical role of cryopyrin in host defense mechanisms and provide insights into the pathogenesis of autoinflammatory syndromes.The study investigates the role of cryopyrin (Nalp3) in the activation of caspase-1 and the production of inflammatory cytokines IL-1β and IL-18. Cryopyrin deficiency in mice results in the inability to activate caspase-1 and produce IL-1β and IL-18 in response to bacterial RNA and synthetic compounds R837 and R848. However, other inflammatory cytokines such as TNF-α and IL-6, as well as the activation of NF-κB and MAPKs, are unaffected. The study also shows that Toll-like receptors (TLRs) and cryopyrin control the secretion of IL-1β and IL-18 through different intracellular pathways. These findings highlight the critical role of cryopyrin in host defense mechanisms and provide insights into the pathogenesis of autoinflammatory syndromes.