C02N

Regulation of NLRP3 inflammasome licensing in autoinflammation

Project Summary

Aberrant NLRP3 inflammasome activity contributes to pathogenesis in numerous acquired and hereditary diseases including CAPS. Posttranslational NLRP3 licensing events are promising targets for the specific modulation of inflammasome activity without interfering with other immune mechanisms. Using molecular, cellular and in vivo methods and disease models, the project will systematically analyse the ability of specific cytokines to influence licensing, as well as the cell types that are the primary culprits in NLRP3-related pathology. These studies will help identify rational approaches to reprogram immune responses to re-establish control over NLRP3 activity.