Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling.
dc.contributor.author | Puttur, Franz | |
dc.contributor.author | Francozo, Marcela | |
dc.contributor.author | Solmaz, Gülhas | |
dc.contributor.author | Bueno, Carlos | |
dc.contributor.author | Lindenberg, Marc | |
dc.contributor.author | Gohmert, Melanie | |
dc.contributor.author | Swallow, Maxine | |
dc.contributor.author | Tufa, Dejene | |
dc.contributor.author | Jacobs, Roland | |
dc.contributor.author | Lienenklaus, Stefan | |
dc.contributor.author | Kühl, Anja A | |
dc.contributor.author | Borkner, Lisa | |
dc.contributor.author | Cicin-Sain, Luka | |
dc.contributor.author | Holzmann, Bernard | |
dc.contributor.author | Wagner, Hermann | |
dc.contributor.author | Berod, Luciana | |
dc.contributor.author | Sparwasser, Tim | |
dc.date.accessioned | 2016-11-18T12:05:57Z | |
dc.date.available | 2016-11-18T12:05:57Z | |
dc.date.issued | 2016-10-18 | |
dc.identifier.citation | Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. 2016, 17 (4):1113-1127 Cell Rep | en |
dc.identifier.issn | 2211-1247 | |
dc.identifier.pmid | 27760315 | |
dc.identifier.doi | 10.1016/j.celrep.2016.09.055 | |
dc.identifier.uri | http://hdl.handle.net/10033/620588 | |
dc.description.abstract | Cytomegalovirus (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.language | ENG | |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.title | Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. | |
dc.type | Article | en |
dc.contributor.department | Twincore 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.journal | Cell reports | en |
refterms.dateFOA | 2018-06-12T21:50:30Z | |
html.description.abstract | Cytomegalovirus (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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publications of the TwinCore unit Infection immunology [80]
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