| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Medicine and
Department of Immunology, Duke University Medical Center, Durham, NC 27710
Type I IFN plays an important role in the activation of NK cells. However, the mechanism underlying type I IFN-dependent NK cell activation remains largely unknown. A recent report suggested that type I IFN acted on accessory dendritic cells, leading to IL-15 production, and that subsequent trans-presentation of IL-15 was required for NK cell activation upon stimulation with synthetic TLR ligands. It is not clear how type I IFN regulates NK cell activation in response to live pathogens. Using a murine model of infection with vaccinia virus (VV), we previously demonstrated a critical role for type I IFN in the innate immune control of VV infection. In this study, we first showed that type I IFN did not directly protect L929 cells from VV infection in vitro and that type I IFN-dependent innate immune control of VV infection in vivo was mediated by activated NK cells. We further demonstrated that direct action of type I IFN on NK cells, but not on dendritic cells, is required for the activation of NK cells in response to VV infection both in vitro and in vivo, leading to efficient VV clearance. Our findings may help design effective strategies for the control of poxviral infections in vivo.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants CA111807 and CA047741 (to Y.Y.), and an Alliance for Cancer Gene Therapy grant (to Y.Y.).
2 Address correspondence and reprint requests to Dr. Yiping Yang, Departments of Medicine and Immunology, Duke University Medical Center, Box 103005, Durham, NC 27710. E-mail address: yang0029{at}mc.duke.edu
3 Abbreviations used in this paper: VV, vaccinia virus; IFN
βR1, IFN-β receptor 1; DC, dendritic cell; WT, wild type; EMCV, encephalomyocardititis virus; MOI, multiplicity of infection; MCMV, murine cytomegalovirus.
This article has been cited by other articles:
|
|
 |
|
  C. Bourquin, L. Schmidt, A.-L. Lanz, B. Storch, C. Wurzenberger, D. Anz, N. Sandholzer, R. Mocikat, M. Berger, H. Poeck, et al. Immunostimulatory RNA Oligonucleotides Induce an Effective Antitumoral NK Cell Response through the TLR7 J. Immunol., November 15, 2009; 183(10): 6078 - 6086. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Miyake, Y. Kumagai, H. Kato, Z. Guo, K. Matsushita, T. Satoh, T. Kawagoe, H. Kumar, M. H. Jang, T. Kawai, et al. Poly I:C-Induced Activation of NK Cells by CD8{alpha}+ Dendritic Cells via the IPS-1 and TRIF-Dependent Pathways J. Immunol., August 15, 2009; 183(4): 2522 - 2528. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Myskiw, J. Arsenio, R. van Bruggen, Y. Deschambault, and J. Cao Vaccinia Virus E3 Suppresses Expression of Diverse Cytokines through Inhibition of the PKR, NF-{kappa}B, and IRF3 Pathways J. Virol., July 1, 2009; 83(13): 6757 - 6768. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. H. Mogensen Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses Clin. Microbiol. Rev., April 1, 2009; 22(2): 240 - 273. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. M. Ngoi, M. G. Tovey, and A. T. Vella Targeting Poly(I:C) to the TLR3-Independent Pathway Boosts Effector CD8 T Cell Differentiation through IFN-{alpha}/{beta} J. Immunol., December 1, 2008; 181(11): 7670 - 7680. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
