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dc.contributor.authorPuttur, Franz
dc.contributor.authorFrancozo, Marcela
dc.contributor.authorSolmaz, Gülhas
dc.contributor.authorBueno, Carlos
dc.contributor.authorLindenberg, Marc
dc.contributor.authorGohmert, Melanie
dc.contributor.authorSwallow, Maxine
dc.contributor.authorTufa, Dejene
dc.contributor.authorJacobs, Roland
dc.contributor.authorLienenklaus, Stefan
dc.contributor.authorKühl, Anja A
dc.contributor.authorBorkner, Lisa
dc.contributor.authorCicin-Sain, Luka
dc.contributor.authorHolzmann, Bernard
dc.contributor.authorWagner, Hermann
dc.contributor.authorBerod, Luciana
dc.contributor.authorSparwasser, Tim
dc.date.accessioned2016-11-18T12:05:57Z
dc.date.available2016-11-18T12:05:57Z
dc.date.issued2016-10-18
dc.identifier.citationConventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. 2016, 17 (4):1113-1127 Cell Repen
dc.identifier.issn2211-1247
dc.identifier.pmid27760315
dc.identifier.doi10.1016/j.celrep.2016.09.055
dc.identifier.urihttp://hdl.handle.net/10033/620588
dc.description.abstractCytomegalovirus (CMV) is an opportunistic virus severely infecting immunocompromised individuals. In mice, endosomal Toll-like receptor 9 (TLR9) and downstream myeloid differentiation factor 88 (MyD88) are central to activating innate immune responses against mouse CMV (MCMV). In this respect, the cell-specific contribution of these pathways in initiating anti-MCMV immunity remains unclear. Using transgenic mice, we demonstrate that TLR9/MyD88 signaling selectively in CD11c(+) dendritic cells (DCs) strongly enhances MCMV clearance by boosting natural killer (NK) cell CD69 expression and IFN-γ production. In addition, we show that in the absence of plasmacytoid DCs (pDCs), conventional DCs (cDCs) promote robust NK cell effector function and MCMV clearance in a TLR9/MyD88-dependent manner. Simultaneously, cDC-derived IL-15 regulates NK cell degranulation by TLR9/MyD88-independent mechanisms. Overall, we compartmentalize the cellular contribution of TLR9 and MyD88 signaling in individual DC subsets and evaluate the mechanism by which cDCs control MCMV immunity.
dc.languageENG
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleConventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling.
dc.typeArticleen
dc.contributor.departmentTwincore Centre of Experimental and Clinical Infection Research; a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover 30625, Germany.en
dc.identifier.journalCell reportsen
refterms.dateFOA2018-06-12T21:50:30Z
html.description.abstractCytomegalovirus (CMV) is an opportunistic virus severely infecting immunocompromised individuals. In mice, endosomal Toll-like receptor 9 (TLR9) and downstream myeloid differentiation factor 88 (MyD88) are central to activating innate immune responses against mouse CMV (MCMV). In this respect, the cell-specific contribution of these pathways in initiating anti-MCMV immunity remains unclear. Using transgenic mice, we demonstrate that TLR9/MyD88 signaling selectively in CD11c(+) dendritic cells (DCs) strongly enhances MCMV clearance by boosting natural killer (NK) cell CD69 expression and IFN-γ production. In addition, we show that in the absence of plasmacytoid DCs (pDCs), conventional DCs (cDCs) promote robust NK cell effector function and MCMV clearance in a TLR9/MyD88-dependent manner. Simultaneously, cDC-derived IL-15 regulates NK cell degranulation by TLR9/MyD88-independent mechanisms. Overall, we compartmentalize the cellular contribution of TLR9 and MyD88 signaling in individual DC subsets and evaluate the mechanism by which cDCs control MCMV immunity.


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