Journal article

Cutting Edge: miR-223 and EBV miR-BART15 Regulate the NLRP3 Inflammasome and IL-1 beta Production

Moritz Haneklaus, Motti Gerlic, Mariola Kurowska-Stolarska, Ashleigh-Ann Rainey, Dagmar Pich, Iain B McInnes, Wolfgang Hammerschmidt, Luke AJ O'Neill, Seth L Masters

The Journal of Immunology | AMER ASSOC IMMUNOLOGISTS | Published : 2012

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 ..

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University of Melbourne Researchers

Grants

Awarded by National Health and Medical Research Council Overseas Biomedical Fellowship


Awarded by Versus Arthritis


Funding Acknowledgements

S.L.M. was supported by a National Health and Medical Research Council Overseas Biomedical Fellowship (516783) and a Victorian Endowment for Science, Knowledge and Innovation Fellowship. M.K.-S. was supported by an Arthritis Research United Kingdom Career Development Grant. A.-A.R. was supported by the Oliver Bird Foundation. Trinity College Dublin was supported by Science Foundation Ireland.