Figure 2.

Potential inflammasome targets for novel PF therapeutics. Lysosomal membrane permeabilization plays an important role in cathepsin B release and inflammasome activation. Therefore, stabilization of the lysosomal membrane would prevent initiation of the adverse events associated with inflammasome activation. Similarly, inhibition of cathepsin B would attenuate inflammasome assembly and activation. Further downstream of inflammasome assembly, inhibition of caspase -1, would prevent maturation of proinflammatory cytokines such as IL-1β and IL-18. In addition, IL- 1R antagonists would prevent the downstream events following the binding of IL-1β to its receptor.