Fig. 4.
Activation of IL-1β by inflammasomes and other pathways. The three types of inflammasome shown here can recruit caspase-1, which converts pro-IL-1β into the mature form, IL-1β. (A) MDP, R837, R848, bacterial RNA, DNA viruses and several intracellular bacteria activate the NALP3 inflammasome. NALP3 forms a complex with the adapters ASC and CARDINAL to recruit caspase-1. (B) Extracellular ATP activates the P2X7 purine receptor, which then helps to allow the pannexin-1 receptor to cause K+ efflux, which enhances activation of the NALP3 (and NALP1) inflammasome. (C) Some microbial toxins, and (D) gout-associated uric acid crystals, calcium pyrophosphate dihydrate crystals (CPPD), UV-B irradiation, alum, silica, asbestos and amyloid-β also induce activation of the NALP3 inflammasome. These stimuli induce ROS production or release of cathepsins during lysosome rupture. (E) Flagellin activates IPAF and NAIP5. The IPAF inflammasome recruits ASC and caspase-1. (F) The NALP1 inflammasome senses Bacillus anthrax LT and activates caspase-1 via ASC. (G) TLR ligands also induce the synthesis of pro-IL-1β.