NOD-like receptors P3 is activated upon exposure to whole pathogens, but also by a number of host-derived danger signals, which are indicative of not only tissue injury (DAMPs), but also environmental irritants (Schroder and Tschopp, 2010). Mutation of NLRP3 is responsible for rare autoinflammatory diseases, collectively referred to as cryopyrin-associated periodic syndromes (CAPS; Neven et al., 2004; Ting and Davis, 2005; Jha and Ting, 2009), characterized by the hyperactivation of the inflammasome complex and increased IL-1β (Neven et al., 2004; Goldbach-Mansky et al., 2006). In addition, there is emerging evidence for the participation of the NLRP3 inflammasome as a sensor of metabolic stress (i.e., De Nardo and Latz, 2011), demyelination, and it is also involved in some neurodegenerative disorders such as the multiple sclerosis model (Jha et al., 2010) and Alzheimer’s disease (Heneka et al., 2013; Sheedy et al., 2013; Tan et al., 2013).
