Artículo

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" (2016) Cell Reports. 17(4):1113-1127
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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. © 2016 The Authors

Registro:

Documento: Artículo
Título:Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling
Autor: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.
Filiación:Institute of Infection Immunology, Centre for Experimental and Clinical Infection Research (Twincore), Hannover Medical School (MHH) and Helmholtz Centre for Infection Research (HZI)Hannover 30625, Germany
Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes 3900, Ribeirão Preto, São Paulo 14049-900, Brazil
Laboratorio de Virología, Departamento de Química Biológica, IQUIBICEN, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad UniversitariaBuenos Aires C1428EGA, Argentina
Department of Clinical Immunology and Rheumatology, MHHHannover 30625, Germany
Institute for Laboratory Animal Science, MHH, Carl-Neuberg-Strasse 1Hannover 30625, Germany
Institute for Experimental Infection Research, Twincore, MHH, HZI, Feodor-Lynen-Strasse 7Hannover 30625, Germany
Medical Department (Gastroenterology, Infectious Diseases and Rheumatology)/Research Center ImmunoScience, Charité–Universitätsmedizin Berlin, Campus Benjamin FranklinBerlin 12200, Germany
Department for Vaccinology/Immune Aging and Chronic Infection, HZIBraunschweig 38124, Germany
Department of Surgery, Technische Universität MünchenMunich 81675, Germany
Institute for Medical Microbiology, Immunology and Hygiene, Technische Universität MünchenMunich 81675, Germany
Palabras clave: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
Año:2016
Volumen:17
Número:4
Página de inicio:1113
Página de fin:1127
DOI: http://dx.doi.org/10.1016/j.celrep.2016.09.055
Título revista:Cell Reports
Título revista abreviado:Cell Rep.
ISSN:22111247
CAS:gamma interferon, 82115-62-6; toll like receptor 9, 352486-49-8, 390883-32-6; Antiviral Agents; CD11c Antigen; Interferon-gamma; Myeloid Differentiation Factor 88; Toll-Like Receptor 9
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_22111247_v17_n4_p1113_Puttur

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Citas:

---------- APA ----------
Puttur, F., Francozo, M., Solmaz, G., Bueno, C., Lindenberg, M., Gohmert, M., Swallow, M.,..., Sparwasser, T. (2016) . Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. Cell Reports, 17(4), 1113-1127.
http://dx.doi.org/10.1016/j.celrep.2016.09.055
---------- CHICAGO ----------
Puttur, F., Francozo, M., Solmaz, G., Bueno, C., Lindenberg, M., Gohmert, M., et al. "Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling" . Cell Reports 17, no. 4 (2016) : 1113-1127.
http://dx.doi.org/10.1016/j.celrep.2016.09.055
---------- MLA ----------
Puttur, F., Francozo, M., Solmaz, G., Bueno, C., Lindenberg, M., Gohmert, M., et al. "Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling" . Cell Reports, vol. 17, no. 4, 2016, pp. 1113-1127.
http://dx.doi.org/10.1016/j.celrep.2016.09.055
---------- VANCOUVER ----------
Puttur, F., Francozo, M., Solmaz, G., Bueno, C., Lindenberg, M., Gohmert, M., et al. Conventional Dendritic Cells Confer Protection against Mouse Cytomegalovirus Infection via TLR9 and MyD88 Signaling. Cell Rep. 2016;17(4):1113-1127.
http://dx.doi.org/10.1016/j.celrep.2016.09.055