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von Gamm, Matthias; Schaub, Annalisa; Jones, Alisha N; Wolf, Christine; Behrens, Gesine; Lichti, Johannes; Essig, Katharina; Macht, Anna; Pircher, Joachim; Ehrlich, Andreas; Davari, Kathrin; Chauhan, Dhruv; Busch, Benjamin; Wurst, Wolfgang; Feederle, Regina; Feuchtinger, Annette; Tschöp, Matthias H; Friedel, Caroline C; Hauck, Stefanie M; Sattler, Michael; Geerlof, Arie; Hornung, Veit; Heissmeyer, Vigo; Schulz, Christian; Heikenwalder, Mathias; Glasmacher, Elke
The Journal of experimental medicine, 07/2019, Letnik: 216, Številka: 7Journal Article
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 -deficient mice, which develop hypertrophic lymph nodes. We used various mice with immune cell-specific deletions of to demonstrate that Regnase-3 acts specifically within myeloid cells. 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 ( ), 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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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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