Gout: new insights into an old disease
J. Clin. Invest. Fabio Martinon, et al. 116:2073 doi:10.1172/JCI29404 [Go to this article.]

Figure 1
Model of the role of IL-1β in gouty inflammation. MSU crystals internalized by monocytes activate the NALP3 inflammasome (Phase 1, lower left). NALP3 protein activation leads to the recruitment and activation of the adaptor ASC and caspase-1 via PYD-PYD and CARD-CARD homotypic interactions, resulting in the processing and maturation of pro–IL-1β into its biologically active form, IL-1β. IL-1β (mainly acting on nonleukocytic cell types, possibly synoviocytes) will then activate the IL-1R complex, leading to recruitment of MyD88 via TIR-TIR homotypic interactions. This results in the activation of NF-κB, which will turn on the transcription of neutrophil-recruiting chemokines, such as IL-8, S100, or macrophage inflammatory protein 2 (MIP-2) (Phase 2, lower right). ASC, apoptosis-associated speck-like protein containing a CARD; CARD, caspase-recruitment domain; DD, death domain; PYD, pyrin domain.