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Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection.

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Date
2010-03-12
Authors
Martinez, Jennifer
Huang, Xiaopei
Yang, Yiping
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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.
Type
Journal article
Subject
Animals
Cells, Cultured
Dendritic Cells
Extracellular Signal-Regulated MAP Kinases
Interleukin-12
Interleukin-6
Killer Cells, Natural
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Myeloid Differentiation Factor 88
NK Cell Lectin-Like Receptor Subfamily K
Phosphatidylinositol 3-Kinases
Receptors, Interleukin-1
Signal Transduction
Toll-Like Receptor 2
Vaccinia
Vaccinia virus
Permalink
https://hdl.handle.net/10161/4596
Published Version (Please cite this version)
10.1371/journal.ppat.1000811
Publication Info
Martinez, Jennifer; Huang, Xiaopei; & Yang, Yiping (2010). Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection. PLoS Pathog, 6(3). pp. e1000811. 10.1371/journal.ppat.1000811. Retrieved from https://hdl.handle.net/10161/4596.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Huang

Xiaopei Huang

Assistant Professor in Medicine
Yang

Yiping Yang

Professor of Medicine
The goal of Dr. Yang’s laboratory is to understand the molecular and cellular mechanisms leading to the generation of potent and long-lasting anti-tumor immunity, and to develop effective gene immunotherapeutic strategies for treating cancer. Furthermore, rational pre-clinical approaches will be tested in clinical trials in patients with Epstein-Barr virus (EBV)-related malignancies. Specifically, we focus on the following areas: 1. Innate Immunity to Viruses. Reco
Alphabetical list of authors with Scholars@Duke profiles.
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