Fig. 3.

Inflammasome activation and pyroptosis signaling. Components of the bacterial T3SS and bacterial flagellins can activate the NAIPs. In turn, NAIPs stimulate the NLRC-4 inflammasome (top left), leading to caspase-1 activation. Anthrax lethal toxin (top middle) directly interacts with NLRP1b and triggers the recruitment of ASC. Intracellular perturbations culminating in potassium efflux stimulate the assembly of the NLRP3 inflammasome (top right), leading to the recruitment of the adaptor protein ASC. NLRP3 requires priming signals via the ligation of TNF or TLRs. The IFN-stimulated GBPs facilitate the release of the pathogenic DNA fragments into the cytosol, which in turn can stimulate the AIM2 inflammasome. Caspase-11 and caspase-4/5 (left) can directly detect LPS, released by the GBPs into the cytosol. Active caspase-1 can process pro-IL1β/IL18 and cleave GSDMD, subsequently leading to GSDMD pore formation and release of the ILs into the extracellular space.