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. Author manuscript; available in PMC: 2021 Jun 19.
Published in final edited form as: Circ Res. 2020 Jun 18;127(1):73–90. doi: 10.1161/CIRCRESAHA.119.316364

Figure 1. Mechanisms responsible for the activation of NLRP3 inflammasome in immune cells via the two basic steps: ‘priming’ and ‘triggering’ processes.

Figure 1.

Pharmacological treatments directed at 1) ‘Priming’ stimuli (with IL-1R inhibitor anakinra and TNFα receptor inhibitor etanercept), 2) ‘Triggering’ stimuli (with P2X7R inhibitor AZD9056), 3) NLRP3 (with MCC950 and colchicine), and 4) the effectors capase-1 (with VX-765) and IL-1β (with canakinumab). ASC, apoptosis-associated speck-like protein containing a CARD; DAMPs, damage-associated molecular patterns; GSDMD, gesdermin-D; IL-1R, interleukin-1 receptor; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; NLRP3, NACHT, LRR and PYD domain containing protein 3; Nt-GSDMD, N-terminus fragment of gesdermin-D; mtROS, mitochondrial ROS; PAMPs, pathogen-associated molecular patterns; P2X7R, purinergic receptor P2X7R; TLR, toll-like receptor.