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Review
. 2012 Dec 25;64(6):741-50.

[Regulation of NOD like receptors and inflammasome during the inflammation]

[Article in Chinese]
An-Nan Liu  1 , Tie-Ying Sun
Affiliations
  • PMID: 23258340
Free article
Review

[Regulation of NOD like receptors and inflammasome during the inflammation]

[Article in Chinese]
An-Nan Liu et al. Sheng Li Xue Bao. .
Free article

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.

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