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Cell Mol Life Sci. 2016 Jun;73(11-12):2335-47. doi: 10.1007/s00018-016-2204-3. Epub 2016 Apr 5.

Inflammasomes as polyvalent cell death platforms.

Author information

1
NOD-like Receptor and Inflammasome Laboratory, Inflammation Research Center, VIB, Technologiepark 927, B-9052, Zwijnaarde, Belgium.
2
Department of Internal Medicine, Ghent University, B-9000, Ghent, Belgium.
3
NOD-like Receptor and Inflammasome Laboratory, Inflammation Research Center, VIB, Technologiepark 927, B-9052, Zwijnaarde, Belgium. mohamed.lamkanfi@irc.vib-ugent.be.
4
Department of Internal Medicine, Ghent University, B-9000, Ghent, Belgium. mohamed.lamkanfi@irc.vib-ugent.be.

Abstract

Inflammasomes are multi-protein platforms that are organized in the cytosol to cope with pathogens and cellular stress. The pattern recognition receptors NLRP1, NLRP3, NLRC4, AIM2 and Pyrin all assemble canonical platforms for caspase-1 activation, while caspase-11-dependent inflammasomes respond to intracellular Gram-negative pathogens. Inflammasomes are chiefly known for their roles in maturation and secretion of the inflammatory cytokines interleukin-(IL)1β and IL18, but they can also induce regulated cell death. Activation of caspases 1 and 11 in myeloid cells can trigger pyroptosis, a lytic and inflammatory cell death mode. Pyroptosis has been implicated in secretion of IL1β, IL18 and intracellular alarmins. Akin to these factors, it may have beneficial roles in controlling pathogen replication, but become detrimental in the context of chronic autoinflammatory diseases. Inflammasomes are increasingly implicated in induction of additional regulated cell death modes such as pyronecrosis and apoptosis. In this review, we overview recent advances in inflammasome-associated cell death research, illustrating the polyvalent roles of these macromolecular platforms in regulated cell death signaling.

KEYWORDS:

Apoptosis; Caspase-1; Caspase-11; Cell death; Inflammasome; Inflammation; Pyroptosis

PMID:
27048821
DOI:
10.1007/s00018-016-2204-3
[Indexed for MEDLINE]

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