Figure 1.
The prototypical NLRP3 and NLRC4 inflammasomes.
(A) The NLRP3 inflammasome is activated by both bacterial (e.g., MDP, bacterial RNA, β-glucan), exogenous (e.g., silica, alum), and endogenous (e.g., uric acid cristals, ATP) stimuli. (B) The NLRC4 inflammasome is activated by flagellin in a TLR5-independent fashion.
Figure 2.
Diagram representing the differential caspase-1/IL-1β activation pathways in monocytes and macrophages.
Caspase-1 is constitutively activated in monocytes, and these cells release mature IL-1β after single stimulation with TLR ligands. IL-1β secretion is induced by endogenously-released ATP. In contrast, macrophages need a double stimulation: one stimulus (TLR-ligands) induces transcription, and a second stimulus (ATP) induces IL-1β secretion.
Table 1.
Susceptibility to In Vivo Experimental Models of Infection in Mice Deficient in IL-1β, IL-18, or Inflammasome Components.
Figure 3.
Inflammasome-independent processing of pro-IL-1β.
In addition to caspase-1-dependent activation, pro-IL-1β can also be processed by neutrophil-derived serine proteases, or pathogen-derived proteases.