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von Gamm, M. ; Schaub, A. ; Jones, A. ; Wolf, C. ; Behrens, G.* ; Lichti, J. ; Essig, K.* ; Macht, A. ; Pircher, J.* ; Ehrlich, A.* ; Davari, K.* ; Chauhan, D.* ; Busch, B.* ; Wurst, W. ; Feederle, R. ; Feuchtinger, A. ; Tschöp, M.H. ; Friedel, C.C.* ; Hauck, S.M. ; Sattler, M. ; Geerlof, A. ; Hornung, V.* ; Heissmeyer, V. ; Schulz, C.* ; Heikenwalder, M.* ; Glasmacher, E.

Immune homeostasis and regulation of the interferon pathway require myeloid-derived Regnase-3.

J. Exp. Med. 216, 1700-1723 (2019)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
The RNase Regnase-1 is a master RNA regulator in macrophages and T cells that degrades cellular and viral RNA upon NF-κB signaling. The roles of its family members, however, remain largely unknown. Here, we analyzed Regnase-3-deficient mice, which develop hypertrophic lymph nodes. We used various mice with immune cell-specific deletions of Regnase-3 to demonstrate that Regnase-3 acts specifically within myeloid cells. Regnase-3 deficiency systemically increased IFN signaling, which increased the proportion of immature B and innate immune cells, and suppressed follicle and germinal center formation. Expression analysis revealed that Regnase-3 and Regnase-1 share protein degradation pathways. Unlike Regnase-1, Regnase-3 expression is high specifically in macrophages and is transcriptionally controlled by IFN signaling. Although direct targets in macrophages remain unknown, Regnase-3 can bind, degrade, and regulate mRNAs, such as Zc3h12a (Regnase-1), in vitro. These data indicate that Regnase-3, like Regnase-1, is an RNase essential for immune homeostasis but has diverged as key regulator in the IFN pathway in macrophages.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Nf-kappa-b; Helper T-cells; Messenger-rna; Gene-expression; Roquin; Family; Inflammation; Macrophages; Microrna; Innate
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Zeitschrift Journal of Experimental Medicine
Quellenangaben Band: 216, Heft: 7, Seiten: 1700-1723 Artikelnummer: , Supplement: ,
Verlag Rockefeller University Press
Verlagsort 950 Third Ave, 2nd Flr, New York, Ny 10022 Usa
Begutachtungsstatus