Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6132327 | Current Opinion in Microbiology | 2013 | 8 Pages |
Abstract
Cell death is an effective strategy to limit intracellular infections. Canonical inflammasomes, including NLRP3, NLRC4, and AIM2, recruit and activate caspase-1 in response to a range of microbial stimuli and endogenous danger signals. Caspase-1 then promotes the secretion of IL-1β and IL-18 and a rapid form of lytic programmed cell death termed pyroptosis. A second inflammatory caspase, mouse caspase-11, mediates pyroptotic death through an unknown non-canonical inflammasome system in response to cytosolic bacteria. In addition, recent work shows that inflammasomes can also recruit procaspase-8, initiating apoptosis. The induction of multiple pathways of cell death has probably evolved to counteract microbial evasion of cell death pathways.
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Authors
Youssef Aachoui, Vitaliya Sagulenko, Edward A Miao, Katryn J Stacey,