Inflammasome priming in sterile inflammatory disease
- Author(s)
- Patel, MN; Carroll, RG; Galvan-Pena, S; Mills, EL; Olden, R; Triantafilou, M; Wolf, AI; Bryant, CE; Triantafilou, K; Masters, SL;
- Details
- Publication Year 2017-02,Volume 23,Issue #2,Page 165-180
- Journal Title
- Trends Mol Med
- Publication Type
- Journal Article
- Abstract
- The inflammasome is a cytoplasmic protein complex that processes interleukins (IL)-1beta 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-1beta, 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.
- Publisher
- Cell Press
- Research Division(s)
- Inflammation
- PubMed ID
- 28109721
- Publisher's Version
- https://doi.org/10.1016/j.molmed.2016.12.007
- NHMRC Grants
- NHMRC/1057815, NHMRC/1099262,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2017-04-06 09:27:28
Last Modified: 2017-04-07 02:55:55