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. 2021 Dec 3;12:797110. doi: 10.3389/fphar.2021.797110

FIGURE 1.

FIGURE 1

Overview of five inflammasome complexes. NLRP1 undergoes autocatalytic processing in its FIIND followed by proteasomal degradation of its autoinhibitory N-terminus to engage caspase-1 in the C-terminal CARD for its activation. NAIPs are necessary for NLRC4 inflammasome activation to recognize S. typhimurium. In NLRP1 and NLRC4 activation events, caspase-1 can be directly recruited independently of the adapter ASC. The NLRP3 inflammasome can be activated by a broad spectrum of exogenous and endogenous stimuli. AIM2 activation requires dsDNA of microbial or host origin in the cytosol. Toxin-induced modifications of Rho GTPases reduce the phosphorylation of pyrin, which promotes the assembly of the pyrin inflammasome. NLRP3, AIM2, and pyrin activation events all require the adaptor ASC to activate caspase-1. Finally, activated caspase-1 drives gasdermin D cleavage to release the N-terminus, which forms the gasdermin D pore and drives pyroptosis. At the same time, activated caspase-1 cleaves pro-IL-1β to mature IL-1β into the extracellular matrix.