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dc.contributor.author Martinez, J
dc.contributor.author Huang, X
dc.contributor.author Yang, Y
dc.coverage.spatial United States
dc.date.accessioned 2011-06-21T17:32:22Z
dc.date.issued 2010-03
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/20300608
dc.identifier.citation PLoS Pathog, 2010, 6 (3), pp. e1000811 - ?
dc.identifier.uri http://hdl.handle.net/10161/4596
dc.description.abstract Natural killer (NK) cells play an essential role in innate immune control of poxviral infections in vivo. However, the mechanism(s) underlying NK cell activation and function in response to poxviruses remains poorly understood. In a mouse model of infection with vaccinia virus (VV), the most studied member of the poxvirus family, we identified that the Toll-like receptor (TLR) 2-myeloid differentiating factor 88 (MyD88) pathway was critical for the activation of NK cells and the control of VV infection in vivo. We further showed that TLR2 signaling on NK cells, but not on accessory cells such as dendritic cells (DCs), was necessary for NK cell activation and that this intrinsic TLR2-MyD88 signaling pathway was required for NK cell activation and played a critical role in the control of VV infection in vivo. In addition, we showed that the activating receptor NKG2D was also important for efficient NK activation and function, as well as recognition of VV-infected targets. We further demonstrated that VV could directly activate NK cells via TLR2 in the presence of cytokines in vitro and TLR2-MyD88-dependent activation of NK cells by VV was mediated through the phosphatidylinositol 3-kinase (PI3K)-extracellular signal-regulated kinase (ERK) pathway. Taken together, these results represent the first evidence that intrinsic TLR signaling is critical for NK cell activation and function in the control of a viral infection in vivo, indicate that multiple pathways are required for efficient NK cell activation and function in response to VV infection, and may provide important insights into the design of effective strategies to combat poxviral infections.
dc.format.extent e1000811 - ?
dc.language eng
dc.language.iso en_US en_US
dc.relation.ispartof PLoS Pathog
dc.relation.isversionof 10.1371/journal.ppat.1000811
dc.subject Animals
dc.subject Cells, Cultured
dc.subject Dendritic Cells
dc.subject Extracellular Signal-Regulated MAP Kinases
dc.subject Interleukin-12
dc.subject Interleukin-6
dc.subject Killer Cells, Natural
dc.subject Lymphocyte Activation
dc.subject Mice
dc.subject Mice, Inbred C57BL
dc.subject Mice, Mutant Strains
dc.subject Myeloid Differentiation Factor 88
dc.subject NK Cell Lectin-Like Receptor Subfamily K
dc.subject Phosphatidylinositol 3-Kinases
dc.subject Receptors, Interleukin-1
dc.subject Signal Transduction
dc.subject Toll-Like Receptor 2
dc.subject Vaccinia
dc.subject Vaccinia virus
dc.title Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2010-3-0 en_US
duke.description.endpage e1000811 en_US
duke.description.issue 3 en_US
duke.description.startpage e1000811 en_US
duke.description.volume 6 en_US
dc.relation.journal Plos Pathogens en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/20300608
pubs.issue 3
pubs.organisational-group /Duke
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Immunology
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Cancer Institute
pubs.volume 6
dc.identifier.eissn 1553-7374

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