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Med Sci (Paris). 2018 Jan;34(1):47-53. doi: 10.1051/medsci/20183401013. Epub 2018 Jan 31.

[Regulation of the NLRP3 inflammasome].

[Article in French]

Author information

1
CIRI, Centre international de recherche en infectiologie, université de Lyon, 21, avenue Tony Garnier, 69007 Lyon, France - Inserm, U1111, Lyon, France - École normale supérieure de Lyon, 69000 Lyon, France - Université Lyon 1, Centre international de recherche en infectiologie, 69000 Lyon, France - CNRS, UMR5308, Lyon, France.

Abstract

The innate immunity constitutes an efficient barrier by rapidly detecting pathogens and tissue damages through pattern recognition receptors including NLRP3. Moreover, inappropriate NLRP3 activation causes deleterious inflammation and contributes to various conditions including atherosclerosis, diabetes, gout and Alzheimer's diseases. NLRP3 assembles a multimeric inflammasome complex serving as an activation platform for caspase-1 that controls processing and release of cytosolic inflammatory factors and cytokines including IL-1β Inflammasome assembly is tightly controlled and requires coordinated NLRP3 priming, through cytokine or other pattern recognition receptors, followed by activation by cellular stress. Here, we describe recent advances in the understanding of the signalling pathways supporting the priming and activation of NLRP3, with a special focus on the key role of post-translational modifications of NLRP3, including phosphorylation and ubiquitination, in inflammasome regulation.

PMID:
29384096
DOI:
10.1051/medsci/20183401013
[Indexed for MEDLINE]
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