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. Author manuscript; available in PMC: 2024 Nov 1.
Published in final edited form as: Pharmacol Ther. 2023 Oct 21;251:108545. doi: 10.1016/j.pharmthera.2023.108545

Figure 2. Schematic representation of the NLRP3 activation and the subsequent NLRP3 inflammasome formation.

Figure 2.

(Left) Engagement of TLRs by PAMPs and DAMPs or cytokine receptors by their respective cytokines (IL-1α, IL-1β, or TNFα) lead to upregulation of NFκB-mediated gene expression of inflammasome components, termed priming. (Right) Activation occurs through PAMPs and DAMPs that activate upstream signals resulting in NLRP3 self-oligomerization (in text). NLRP3 then interacts with ASC, pro-caspase-1 is recruited resulting in caspase-1 activation, activated caspase-1 then cleaves pro-IL-1β and pro-IL-18. Biologically active IL-1β and IL-18 are then secreted into the extracellular space. Abbreviations: interleukin-1 alpha (IL-1α), interleukin-1 beta (IL-1β), interleukin 1 receptor 1 (IL-1R1), tumor necrosis factor α (TNFα), tumor necrosis factor receptor (TNFR), toll-like receptor (TLR), damage-associated molecular patterns (DAMPs), pathogen-associated molecular patterns (PAMPS), ATP (adenosine triphosphate), ADP (adenosine diphosphate), GSDMD (gasdermin D), purinergic receptor P2X7 (P2X7R), nuclear factor-κB (NFκB), reactive oxygen species (ROS), apoptosis-associated speck-like protein containing a CARD (ASC).