Transcriptional Regulation of Inflammasomes

被引:60
作者
Cornut, Maxence [1 ]
Bourdonnay, Emilie [1 ]
Henry, Thomas [1 ]
机构
[1] Univ Claude Bernard Lyon 1, Univ Lyon, Inserm U1111, Ctr Int Rech Infectiol CIRI,CNRS,UMR5308,ENS Lyon, F-69007 Lyon, France
关键词
inflammasome; NF-κ B; IRF; NLRP3; caspase-1; epigenetic modification; transcription factor; chromatin; promoter; enhancer; IL-1 RECEPTOR ANTAGONIST; FAMILIAL MEDITERRANEAN FEVER; NLRP3; INFLAMMASOME; KAPPA-B; AIM2; INTERLEUKIN-1-BETA GENE; MOLECULAR-MECHANISMS; BACTERIAL LIGANDS; HUMAN MACROPHAGES; BINDING-PROTEIN;
D O I
10.3390/ijms21218087
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammasomes are multimolecular complexes with potent inflammatory activity. As such, their activity is tightly regulated at the transcriptional and post-transcriptional levels. In this review, we present the transcriptional regulation of inflammasome genes from sensors (e.g., NLRP3) to substrates (e.g., IL-1 beta). Lineage-determining transcription factors shape inflammasome responses in different cell types with profound consequences on the responsiveness to inflammasome-activating stimuli. Pro-inflammatory signals (sterile or microbial) have a key transcriptional impact on inflammasome genes, which is largely mediated by NF-kappa B and that translates into higher antimicrobial immune responses. Furthermore, diverse intrinsic (e.g., circadian clock, metabolites) or extrinsic (e.g., xenobiotics) signals are integrated by signal-dependent transcription factors and chromatin structure changes to modulate transcriptionally inflammasome responses. Finally, anti-inflammatory signals (e.g., IL-10) counterbalance inflammasome genes induction to limit deleterious inflammation. Transcriptional regulations thus appear as the first line of inflammasome regulation to raise the defense level in front of stress and infections but also to limit excessive or chronic inflammation.
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页数:28
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