Journal
JOURNAL OF IMMUNOLOGY
Volume 189, Issue 8, Pages 4175-4181Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1201516
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Funding
- German Research Foundation [SFB704, SFB670]
- European Research Council [ERC-2009-StG 243046]
- University of Bonn (BONFOR)
- Else Kroner-Fresenius Foundation
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Inflammasomes are multiprotein signaling platforms that form upon sensing microbe- or damage-associated molecular patterns. Upon their formation, caspase-1 is activated, leading to the processing of certain proinflammatory cytokines and the initiation of a special type of cell death, known as pyroptosis. Among known inflammasomes, NLRP3 takes on special importance because it appears to be a general sensor of cell stress. Moreover, unlike other inflammasome sensors, NLRP3 inflammasome activity is under additional transcriptional regulation. In this study, we identify the myeloid-specific microRNAmiR-223 as another critical regulator of NLRP3 inflammasome activity. miR-223 suppresses NLRP3 expression through a conserved binding site within the 39 untranslated region of NLRP3, translating to reduced NLRP3 inflammasome activity. Although miR-223 itself is not regulated by proinflammatory signals, its expression varies among different myeloid cell types. Therefore, given the tight transcriptional control of NLRP3 message itself, miR-223 functions as an important rheostat controlling NLRP3 inflammasome activity. The Journal of Immunology, 2012, 189: 4175-4181.
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