Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 103, Issue 2, Pages 233-257Publisher
WILEY
DOI: 10.1189/jlb.3MR0617-250R
Keywords
AIM2; NLRP1; 3; NLRC4; Pyrin; caspases
Categories
Funding
- John Curtin School of Medical Research Ph.D. Scholarship from the Australian National University
- Gretel and Gordon Bootes Foundation
- R. G. Menzies Early Career Fellowship from the National Health and Medical Research Council of Australia
Ask authors/readers for more resources
The inflammasome is a macromolecular protein complex that mediates proteolytic cleavage of pro-IL-1 and -IL-18 and induces cell death in the form of pyroptosis. Certain nucleotide-binding oligomerization domain-like receptors (NLRs), absent in melanoma 2 (AIM2)-like receptors (ALRs), or tripartite motif (TRIM) family receptors trigger the assembly of an inflammasome in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs). Recent studies have revealed a multitude of host components and signals that are essential for controlling canonical and noncanonical inflammasome activation and pyroptosis. These include pore-forming gasdermin proteins, the never in mitosis A-related kinase 7 (NEK7), IFN-inducible proteins (IFIs), reactive oxygen species (ROS), autophagy, potassium efflux, mitochondrial perturbations, and microbial metabolites. Here, we provide a comprehensive overview of the molecular and signaling mechanisms that provide stringent regulation over the activation and effector functions of the inflammasome.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available