Inflammasomes are intracellular macromolecular complexes which represent a major line of innate immune defense. Inflammasome complexes form upon recognition of PAMPs (pathogen-associated molecular patterns) such as  pathogens  or DAMPs (damage-associated molecular patterns) molecules like uric acid which in crystalline form causes gout. Since inflammasomes recognize both PAMPs and DAMPs, their participation in the inflammatory response,  autoinflammation disease states and the adaptive autoimmune response are becoming more of a focus for the development of new anti-inflammatory targets in the treatment of chronic inflammatory disease¹.

The generic structure of the inflammasome  is comprised of an NLR family member, either a NALP or IPAF central protein, an adaptor protein, and a caspase recruitment domain (CARD) to facilitate caspase activation². Perhaps the best studied NALP protein and inflammasome is the NALP3 inflammasome composed of NALP3, ASC, a pyrin protein, Caspase-1,  and Cardinal which facilitates Caspase-1 activation¹.

Inflammasomes mediate caspase activation, particularly Caspase-1. Activation of Caspase-1 leads to cleavage and processing of IL-1b and IL-18 which are then secreted. Both of these cytokines evoke numerous cytokine cascades and both are are associated with infection, inflammation, and autoimmune processes^1,2.

¹Martinon F.,  O. Gaide, V. Petrille, A. Major , and J Tschopp. NALP Inflammasomes: A central role in innate immunity.  Semin. Immunopathol. 29(3): 213-229, 2007.
²Mathews, R.J., M.B. Sprakes, and M.F. McDermott. NOD-Like Receptors and Inflammation. Arthritis Research and Therapy 10(6): 1-14, 2008