Regulation of NOD like receptors and inflammasome during the inflammation.
- Author:
An-Nan LIU
1
;
Tie-Ying SUN
Author Information
1. Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Carrier Proteins;
Caspase 1;
Humans;
Immunity, Innate;
Inflammasomes;
metabolism;
Inflammation;
metabolism;
Interleukin-18;
metabolism;
Interleukin-1beta;
metabolism;
Nod Signaling Adaptor Proteins;
metabolism;
Signal Transduction
- From:
Acta Physiologica Sinica
2012;64(6):741-750
- CountryChina
- Language:Chinese
-
Abstract:
The innate immune system plays a crucial role in the rapid recognition and elimination of invading microbes. Detection of microbes relies on germ-line encoded pattern recognition receptors (PRRs) that recognize essential bacterial molecules, so-called pathogen-associated molecular patterns (PAMPs). A subset of PRRs, belonging to the nucleotide binding oligomerization domain (NOD)-like receptor (NLR) families, detects viral and bacterial pathogens in the cytosol of host cells and induces the assembly of a multi-protein signaling platform called the inflammasome. The inflammasome serves as an activation platform for the cysteine protease Caspase-1, a central mediator of innate immunity. Caspase-1 initiates a novel form of cell death called pyroptosis. Inflammasome activation by pathogen-associated signatures results in the autocatalytic cleavage of Caspase-1 and ultimately leads to the processing and thus secretion of pro-inflammatory cytokines, most importantly interleukin (IL)-1β and IL-18. Here, we review the recent advancements of negative regulatory functions and mechanisms leading to the activation of NLRP1, NLRP3, NLRC4, and AIM2 inflammasomes.
