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. 2019 Dec 13;43(6):349–359. doi: 10.3906/biy-1909-31

Figure 1.

Figure 1

Activation mechanisms of the NLRP3 inflammasome. The NLRP3 inflammasome requires two signals to be activated: the priming signal conferred by stimulation of TLRs by LPS and subsequent induction of inflammasome components’ gene expression through the NFkB pathway and secondly, an activatory signal that triggers the oligomerization of the complex NLRP3 with ASC and Caspase-1; that could be either ROS production by the mitochondria induced by Imiquimod, potassium efflux resulting from ATP or Nigericin stimulation or lysosomal rupture triggered by phagocytosed crystals. The NLRP3 inflammasome is also indirectly activated through the noncanonical inflammasome formed by caspase-4/5 that senses lipopolysaccharide from gram-negative bacteria. LPS: Lipopolysaccharide; TLR: Toll-like receptor; ROS: Recative oxygen species; ATP: Adenosine triphosphate