Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling.

2.50
Hdl Handle:
http://hdl.handle.net/10033/620588
Title:
Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling.
Authors:
Puttur, Franz; Francozo, Marcela; Solmaz, Gülhas; Bueno, Carlos; Lindenberg, Marc; Gohmert, Melanie; Swallow, Maxine; Tufa, Dejene; Jacobs, Roland; Lienenklaus, Stefan; Kühl, Anja A; Borkner, Lisa; Cicin-Sain, Luka; Holzmann, Bernard; Wagner, Hermann; Berod, Luciana; Sparwasser, Tim ( 0000-0001-5645-902X )
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.
Affiliation:
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.
Citation:
Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. 2016, 17 (4):1113-1127 Cell Rep
Journal:
Cell reports
Issue Date:
18-Oct-2016
URI:
http://hdl.handle.net/10033/620588
DOI:
10.1016/j.celrep.2016.09.055
PubMed ID:
27760315
Type:
Article
ISSN:
2211-1247
Appears in Collections:
publications of the TwinCore unit Infection immunology

Full metadata record

DC FieldValue Language
dc.contributor.authorPuttur, Franzen
dc.contributor.authorFrancozo, Marcelaen
dc.contributor.authorSolmaz, Gülhasen
dc.contributor.authorBueno, Carlosen
dc.contributor.authorLindenberg, Marcen
dc.contributor.authorGohmert, Melanieen
dc.contributor.authorSwallow, Maxineen
dc.contributor.authorTufa, Dejeneen
dc.contributor.authorJacobs, Rolanden
dc.contributor.authorLienenklaus, Stefanen
dc.contributor.authorKühl, Anja Aen
dc.contributor.authorBorkner, Lisaen
dc.contributor.authorCicin-Sain, Lukaen
dc.contributor.authorHolzmann, Bernarden
dc.contributor.authorWagner, Hermannen
dc.contributor.authorBerod, Lucianaen
dc.contributor.authorSparwasser, Timen
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.en
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

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