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

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 c...

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Autor principal: Bueno, Carlos Alberto
Publicado: 2016
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22111247_v17_n4_p1113_Puttur
http://hdl.handle.net/20.500.12110/paper_22111247_v17_n4_p1113_Puttur
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spelling paper:paper_22111247_v17_n4_p1113_Puttur2023-06-08T16:35:13Z Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling Bueno, Carlos Alberto conventional DC MCMV NK cells plasmacytoid DC TLR9-MyD88 signaling CD69 antigen gamma interferon glycoprotein p 15095 interleukin 15 myeloid differentiation factor 88 toll like receptor 9 antivirus agent gamma interferon glycoprotein p 15095 myeloid differentiation factor 88 toll like receptor 9 animal cell animal experiment animal model antigen expression Article CD11c+ dendritic cell cell activity cell compartmentalization cell specificity controlled study cytokine production cytomegalovirus infection degranulation dendritic cell effector cell immunoregulation infection prevention innate immunity lymphocyte function mouse natural killer cell nonhuman plasmacytoid dendritic cell priority journal protein function signal transduction transgenic mouse viral clearance animal Bagg albino mouse cytomegalovirus infection cytotoxicity dendritic cell immunology lymphocyte activation metabolism Muromegalovirus physiology virology Animals Antiviral Agents CD11c Antigen Cytomegalovirus Infections Cytotoxicity, Immunologic Dendritic Cells Interferon-gamma Killer Cells, Natural Lymphocyte Activation Mice, Inbred BALB C Muromegalovirus Myeloid Differentiation Factor 88 Signal Transduction Toll-Like Receptor 9 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. © 2016 The Authors Fil:Bueno, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2016 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22111247_v17_n4_p1113_Puttur http://hdl.handle.net/20.500.12110/paper_22111247_v17_n4_p1113_Puttur
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic conventional DC
MCMV
NK cells
plasmacytoid DC
TLR9-MyD88 signaling
CD69 antigen
gamma interferon
glycoprotein p 15095
interleukin 15
myeloid differentiation factor 88
toll like receptor 9
antivirus agent
gamma interferon
glycoprotein p 15095
myeloid differentiation factor 88
toll like receptor 9
animal cell
animal experiment
animal model
antigen expression
Article
CD11c+ dendritic cell
cell activity
cell compartmentalization
cell specificity
controlled study
cytokine production
cytomegalovirus infection
degranulation
dendritic cell
effector cell
immunoregulation
infection prevention
innate immunity
lymphocyte function
mouse
natural killer cell
nonhuman
plasmacytoid dendritic cell
priority journal
protein function
signal transduction
transgenic mouse
viral clearance
animal
Bagg albino mouse
cytomegalovirus infection
cytotoxicity
dendritic cell
immunology
lymphocyte activation
metabolism
Muromegalovirus
physiology
virology
Animals
Antiviral Agents
CD11c Antigen
Cytomegalovirus Infections
Cytotoxicity, Immunologic
Dendritic Cells
Interferon-gamma
Killer Cells, Natural
Lymphocyte Activation
Mice, Inbred BALB C
Muromegalovirus
Myeloid Differentiation Factor 88
Signal Transduction
Toll-Like Receptor 9
spellingShingle conventional DC
MCMV
NK cells
plasmacytoid DC
TLR9-MyD88 signaling
CD69 antigen
gamma interferon
glycoprotein p 15095
interleukin 15
myeloid differentiation factor 88
toll like receptor 9
antivirus agent
gamma interferon
glycoprotein p 15095
myeloid differentiation factor 88
toll like receptor 9
animal cell
animal experiment
animal model
antigen expression
Article
CD11c+ dendritic cell
cell activity
cell compartmentalization
cell specificity
controlled study
cytokine production
cytomegalovirus infection
degranulation
dendritic cell
effector cell
immunoregulation
infection prevention
innate immunity
lymphocyte function
mouse
natural killer cell
nonhuman
plasmacytoid dendritic cell
priority journal
protein function
signal transduction
transgenic mouse
viral clearance
animal
Bagg albino mouse
cytomegalovirus infection
cytotoxicity
dendritic cell
immunology
lymphocyte activation
metabolism
Muromegalovirus
physiology
virology
Animals
Antiviral Agents
CD11c Antigen
Cytomegalovirus Infections
Cytotoxicity, Immunologic
Dendritic Cells
Interferon-gamma
Killer Cells, Natural
Lymphocyte Activation
Mice, Inbred BALB C
Muromegalovirus
Myeloid Differentiation Factor 88
Signal Transduction
Toll-Like Receptor 9
Bueno, Carlos Alberto
Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
topic_facet conventional DC
MCMV
NK cells
plasmacytoid DC
TLR9-MyD88 signaling
CD69 antigen
gamma interferon
glycoprotein p 15095
interleukin 15
myeloid differentiation factor 88
toll like receptor 9
antivirus agent
gamma interferon
glycoprotein p 15095
myeloid differentiation factor 88
toll like receptor 9
animal cell
animal experiment
animal model
antigen expression
Article
CD11c+ dendritic cell
cell activity
cell compartmentalization
cell specificity
controlled study
cytokine production
cytomegalovirus infection
degranulation
dendritic cell
effector cell
immunoregulation
infection prevention
innate immunity
lymphocyte function
mouse
natural killer cell
nonhuman
plasmacytoid dendritic cell
priority journal
protein function
signal transduction
transgenic mouse
viral clearance
animal
Bagg albino mouse
cytomegalovirus infection
cytotoxicity
dendritic cell
immunology
lymphocyte activation
metabolism
Muromegalovirus
physiology
virology
Animals
Antiviral Agents
CD11c Antigen
Cytomegalovirus Infections
Cytotoxicity, Immunologic
Dendritic Cells
Interferon-gamma
Killer Cells, Natural
Lymphocyte Activation
Mice, Inbred BALB C
Muromegalovirus
Myeloid Differentiation Factor 88
Signal Transduction
Toll-Like Receptor 9
description 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. © 2016 The Authors
author Bueno, Carlos Alberto
author_facet Bueno, Carlos Alberto
author_sort Bueno, Carlos Alberto
title Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
title_short Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
title_full Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
title_fullStr Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
title_full_unstemmed Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
title_sort conventional dendritic cells confer protection against mouse cytomegalovirus infection via tlr9 and myd88 signaling
publishDate 2016
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22111247_v17_n4_p1113_Puttur
http://hdl.handle.net/20.500.12110/paper_22111247_v17_n4_p1113_Puttur
work_keys_str_mv AT buenocarlosalberto conventionaldendriticcellsconferprotectionagainstmousecytomegalovirusinfectionviatlr9andmyd88signaling
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