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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todo:paper_22111247_v17_n4_p1113_Puttur2023-10-03T16:40:29Z Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling Puttur, F. Francozo, M. Solmaz, G. Bueno, C. Lindenberg, M. Gohmert, M. Swallow, M. Tufa, D. Jacobs, R. Lienenklaus, S. Kühl, A.A. Borkner, L. Cicin-Sain, L. Holzmann, B. Wagner, H. Berod, L. Sparwasser, T. 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. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar 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 |
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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 Puttur, F. Francozo, M. Solmaz, G. Bueno, C. Lindenberg, M. Gohmert, M. Swallow, M. Tufa, D. Jacobs, R. Lienenklaus, S. Kühl, A.A. Borkner, L. Cicin-Sain, L. Holzmann, B. Wagner, H. Berod, L. Sparwasser, T. 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 |
| format |
JOUR |
| author |
Puttur, F. Francozo, M. Solmaz, G. Bueno, C. Lindenberg, M. Gohmert, M. Swallow, M. Tufa, D. Jacobs, R. Lienenklaus, S. Kühl, A.A. Borkner, L. Cicin-Sain, L. Holzmann, B. Wagner, H. Berod, L. Sparwasser, T. |
| author_facet |
Puttur, F. Francozo, M. Solmaz, G. Bueno, C. Lindenberg, M. Gohmert, M. Swallow, M. Tufa, D. Jacobs, R. Lienenklaus, S. Kühl, A.A. Borkner, L. Cicin-Sain, L. Holzmann, B. Wagner, H. Berod, L. Sparwasser, T. |
| author_sort |
Puttur, F. |
| 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 |
| url |
http://hdl.handle.net/20.500.12110/paper_22111247_v17_n4_p1113_Puttur |
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