Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Transcriptional Regulation of Inflammasomes

Version 1 : Received: 21 October 2020 / Approved: 23 October 2020 / Online: 23 October 2020 (10:41:25 CEST)

How to cite: Cornut, M.; Bourdonnay, E.; Henry, T. Transcriptional Regulation of Inflammasomes. Preprints 2020, 2020100482 (doi: 10.20944/preprints202010.0482.v1). Cornut, M.; Bourdonnay, E.; Henry, T. Transcriptional Regulation of Inflammasomes. Preprints 2020, 2020100482 (doi: 10.20944/preprints202010.0482.v1).

Abstract

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-1β). 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-κB 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.

Subject Areas

Inflammasome; NF-κB; IRF; NLRP3; caspase-1; epigenetic modification; transcription factor; chromatin; promoter; enhancer

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