NLRP3 inflammasome signaling axis (including IL-1β/IL-1R1/MyD88/NF-kappaB) (NLRP3 (for NLRP3 inflammasome); NF-κB (for nuclear factor kappa-light-chain-enhancer of activated B cells); IL-1R1; MyD88)

The NLRP3 inflammasome is a multi-protein complex assembled in response to pathogen- or danger-associated molecular patterns (PAMPs/DAMPs), primarily within macrophages and other innate immune cells. Upon activation, it promotes the cleavage and release of pro-inflammatory cytokines IL-1β and IL-18 through caspase-1, driving both local and systemic inflammation. Signaling is propagated via IL-1β binding to IL-1R1, recruitment of MyD88, and activation of the NF-κB pathway, leading to transcription of additional inflammatory mediators. Aberrant activation has been implicated in a wide spectrum of auto-inflammatory, neurodegenerative, cardiovascular, and metabolic diseases, making each component a significant therapeutic target[2][3][4][5].

Other names

CryopyrinCIAS1NALP3 inflammasomeInterleukin-1 betaInterleukin-1 receptor type 1Myeloid differentiation primary response 88Nuclear factor kappa-light-chain-enhancer of activated B cells

Direct inhibition of NLRP3 oligomerization/activation\nBlocking IL-1β signaling (canakinumab, anakinra)\nInterfering with upstream priming (NF-κB inhibition)\nInterfering with MyD88-dependent signaling