Myeloid Cells Restrict MCMV and Drive Stress-Induced Extramedullary Hematopoiesis through STAT1.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
AbstractCytomegalovirus (CMV) has a high prevalence worldwide, is often fatal for immunocompromised patients, and causes bone marrow suppression. Deficiency of signal transducer and activator of transcription 1 (STAT1) results in severely impaired antiviral immunity. We have used cell-type restricted deletion of Stat1 to determine the importance of myeloid cell activity for the defense against murine CMV (MCMV). We show that myeloid STAT1 limits MCMV burden and infection-associated pathology in the spleen but does not affect ultimate clearance of infection. Unexpectedly, we found an essential role of myeloid STAT1 in the induction of extramedullary hematopoiesis (EMH). The EMH-promoting function of STAT1 was not restricted to MCMV infection but was also observed during CpG oligodeoxynucleotide-induced sterile inflammation. Collectively, we provide genetic evidence that signaling through STAT1 in myeloid cells is required to restrict MCMV at early time points post-infection and to induce compensatory hematopoiesis in the spleen.
CitationCell Rep. 2019 Feb 26;26(9):2394-2406.e5. doi: 10.1016/j.celrep.2019.02.017.
AffiliationTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH, Feodor-Lynen-Str.7,30625 Hannover, Germany.
The following license files are associated with this item:
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International
- M27 expressed by cytomegalovirus counteracts effective type I interferon induction of myeloid cells but not of plasmacytoid dendritic cells.
- Authors: Döring M, Lessin I, Frenz T, Spanier J, Kessler A, Tegtmeyer P, Dağ F, Thiel N, Trilling M, Lienenklaus S, Weiss S, Scheu S, Messerle M, Cicin-Sain L, Hengel H, Kalinke U
- Issue date: 2014 Dec
- "Activated" STAT proteins: a paradoxical consequence of inhibited JAK-STAT signaling in cytomegalovirus-infected cells.
- Authors: Trilling M, Le VT, Rashidi-Alavijeh J, Katschinski B, Scheller J, Rose-John S, Androsiac GE, Jonjic S, Poli V, Pfeffer K, Hengel H
- Issue date: 2014 Jan 1
- Novel functions of tyrosine kinase 2 in the antiviral defense against murine cytomegalovirus.
- Authors: Strobl B, Bubic I, Bruns U, Steinborn R, Lajko R, Kolbe T, Karaghiosoff M, Kalinke U, Jonjic S, Müller M
- Issue date: 2005 Sep 15
- A role for natural killer T cells and CD1d molecules in counteracting suppression of hematopoiesis in mice induced by infection with murine cytomegalovirus.
- Authors: Broxmeyer HE, Dent A, Cooper S, Hangoc G, Wang ZY, Du W, Gervay-Haque J, Sriram V, Renukaradhya GJ, Brutkiewicz RR
- Issue date: 2007 Apr
- Natural killer cells are required for extramedullary hematopoiesis following murine cytomegalovirus infection.
- Authors: Jordan S, Ruzsics Z, Mitrović M, Baranek T, Arapović J, Krmpotić A, Vivier E, Dalod M, Jonjić S, Dölken L, Koszinowski UH
- Issue date: 2013 May 15