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

Publication ,  Journal Article
Martinez, J; Huang, X; Yang, Y
Published in: PLoS pathogens
March 2010

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.

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Published In

PLoS pathogens

DOI

EISSN

1553-7374

ISSN

1553-7366

Publication Date

March 2010

Volume

6

Issue

3

Start / End Page

e1000811

Related Subject Headings

  • Virology
  • Vaccinia virus
  • Vaccinia
  • Toll-Like Receptor 2
  • Signal Transduction
  • Receptors, Interleukin-1
  • Phosphatidylinositol 3-Kinases
  • NK Cell Lectin-Like Receptor Subfamily K
  • Myeloid Differentiation Factor 88
  • Mice, Mutant Strains
 

Citation

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Martinez, J., Huang, X., & Yang, Y. (2010). Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection. PLoS Pathogens, 6(3), e1000811. https://doi.org/10.1371/journal.ppat.1000811
Martinez, Jennifer, Xiaopei Huang, and Yiping Yang. “Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection.PLoS Pathogens 6, no. 3 (March 2010): e1000811. https://doi.org/10.1371/journal.ppat.1000811.
Martinez, Jennifer, et al. “Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection.PLoS Pathogens, vol. 6, no. 3, Mar. 2010, p. e1000811. Epmc, doi:10.1371/journal.ppat.1000811.

Published In

PLoS pathogens

DOI

EISSN

1553-7374

ISSN

1553-7366

Publication Date

March 2010

Volume

6

Issue

3

Start / End Page

e1000811

Related Subject Headings

  • Virology
  • Vaccinia virus
  • Vaccinia
  • Toll-Like Receptor 2
  • Signal Transduction
  • Receptors, Interleukin-1
  • Phosphatidylinositol 3-Kinases
  • NK Cell Lectin-Like Receptor Subfamily K
  • Myeloid Differentiation Factor 88
  • Mice, Mutant Strains