Cutting edge: miR-223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1 production

Haneklaus, M., Gerlic, M., Kurowska-Stolarska, M. , Rainey, A.-A., Pich, D., McInnes, I.B. , Hammerschmidt, W., O'Neill, L.A.J. and Masters, S.L. (2012) Cutting edge: miR-223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1 production. Journal of Immunology, 189(8), pp. 3795-3799. (doi:10.4049/jimmunol.1200312) (PMID:22984081)

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Abstract

Although microRNA (miRNA) regulation of TLR signaling is well established, this has not yet been observed for NLR proteins or the inflammasomes they form. We have now validated a highly conserved miR-223 target site in the NLRP3 3′-untranslated region. miR-223 expression decreases as monocytes differentiate into macrophages, whereas NLRP3 protein increases during this time. However, overexpression of miR-223 prevents accumulation of NLRP3 protein and inhibits IL-1β production from the inflammasome. Virus inhibition of the inflammasome is an emerging theme, and we have also identified an EBV miRNA that can target the miR-223 binding site in the NLRP3 3′-untranslated region. Furthermore, this virus miRNA can be secreted from infected B cells via exosomes to inhibit the NLRP3 inflammasome in noninfected cells. Therefore, we have identified both the first endogenous miRNA that limits NLRP3 inflammatory capacity during myeloid cell development and also a viral miRNA that takes advantage of this, limiting inflammation for its own purposes.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:McInnes, Professor Iain and Kurowska-Stolarska, Dr Mariola
Authors: Haneklaus, M., Gerlic, M., Kurowska-Stolarska, M., Rainey, A.-A., Pich, D., McInnes, I.B., Hammerschmidt, W., O'Neill, L.A.J., and Masters, S.L.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Journal of Immunology
ISSN:0022-1767
Published Online:14 September 2012

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