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 |
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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 |
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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: | 24 Nov 2024 05:30 |
URI: | https://orca.cardiff.ac.uk/id/eprint/106531 |
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