| First Author | Bauernfeind F | Year | 2012 |
| Journal | J Immunol | Volume | 189 |
| Issue | 8 | Pages | 4175-81 |
| PubMed ID | 22984082 | Mgi Jnum | J:190649 |
| Mgi Id | MGI:5449336 | Doi | 10.4049/jimmunol.1201516 |
| Citation | Bauernfeind F, et al. (2012) NLRP3 inflammasome activity is negatively controlled by miR-223. J Immunol 189(8):4175-81 |
| abstractText | 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 microRNA miR-223 as another critical regulator of NLRP3 inflammasome activity. miR-223 suppresses NLRP3 expression through a conserved binding site within the 3' 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. |
