Inflammasome priming in sterile inflammatory disease

Patel, Meghana N., Carroll, Richard G., Galván-Peña, Silvia, Mills, Evanna L., Olden, Robin, Triantafilou, Martha ORCID: https://orcid.org/0000-0002-8489-2602, Wolf, Amaya I., Bryant, Clare E., Triantafilou, Kathy ORCID: https://orcid.org/0000-0002-7473-6278 and Masters, Seth L. 2017. Inflammasome priming in sterile inflammatory disease. Trends in Molecular Medicine 23 (2) , pp. 165-180. 10.1016/j.molmed.2016.12.007

Preview

PDF - Accepted Post-Print Version Download (660kB) | Preview

Abstract

The inflammasome is a cytoplasmic protein complex that processes interleukins (IL)-1β and IL-18, and drives a form of cell death known as pyroptosis. Oligomerization of this complex is actually the second step of activation, and a priming step must occur first. This involves transcriptional upregulation of pro-IL-1β, inflammasome sensor NLRP3, or the non-canonical inflammasome sensor caspase-11. An additional aspect of priming is the post-translational modification of particular inflammasome constituents. Priming is typically accomplished in vitro using a microbial Toll-like receptor (TLR) ligand. However, it is now clear that inflammasomes are activated during the progression of sterile inflammatory diseases such as atherosclerosis, metabolic disease, and neuroinflammatory disorders. Therefore, it is time to consider the endogenous factors and mechanisms that may prime the inflammasome in these conditions.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Publisher:	Elsevier
ISSN:	1471-4914
Date of First Compliant Deposit:	16 March 2018
Date of Acceptance:	12 December 2016
Last Modified:	07 Nov 2023 16:53
URI:	https://orca.cardiff.ac.uk/id/eprint/106531

Citation Data

Cited 145 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item