Startseite
English
Erweiterte Suche
Durchblättern nach ...
Publikationen im Überblick
Ansprechpartner
Hilfe
DOI
PMC
 |
|
möglich sobald bei der ZB eingereicht worden ist.
Cutting edge: MiR-223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1β production.
J. Immunol. 189, 3795-3799 (2012)
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-1 beta 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. The Journal of Immunology, 2012, 189: 3795-3799.
Altmetric
Weitere Metriken?
Zusatzinfos bearbeiten
[➜Einloggen]
Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
EPSTEIN-BARR-VIRUS; CELLS; ACTIVATION; EXPRESSION; MICRORNAS; RELEASE
ISSN (print) / ISBN
0022-1767
e-ISSN
1550-6606
Zeitschrift
Journal of Immunology
Quellenangaben
Band: 189,
Heft: 8,
Seiten: 3795-3799
Verlag
American Association of Immunologists
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Research Unit Gene Vector (AGV)