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J Mol Biol. 2018 Jan 19;430(2):153-173. doi: 10.1016/j.jmb.2017.10.004. Epub 2017 Oct 10.

COPs and POPs Patrol Inflammasome Activation.

Author information

1
Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
2
Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Robert H. Lurie Comprehensive Cancer Center, Interdepartmental Immunobiology Center and Skin Disease Research Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: c-stehlik@northwestern.edu.
3
Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: a-dorfleutner@northwestern.edu.

Abstract

Sensing and responding to pathogens and tissue damage is a core mechanism of innate immune host defense, and inflammasomes represent a central cytosolic pattern recognition receptor pathway leading to the generation of the pro-inflammatory cytokines interleukin-1β and interleukin-18 and pyroptotic cell death that causes the subsequent release of danger signals to propagate and perpetuate inflammatory responses. While inflammasome activation is essential for host defense, deregulated inflammasome responses and excessive release of inflammatory cytokines and danger signals are linked to an increasing spectrum of inflammatory diseases. In this review, we will discuss recent developments in elucidating the role of PYRIN domain-only proteins (POPs) and the related CARD-only proteins (COPs) in regulating inflammasome responses and their impact on inflammatory disease.

KEYWORDS:

CARD-only protein; Caspase-1; IL-1β; PYD-only protein; inflammasome

PMID:
29024695
PMCID:
PMC5766406
DOI:
10.1016/j.jmb.2017.10.004
[Indexed for MEDLINE]
Free PMC Article

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