Blood online
Home About Blood Authors Subscriptions Permission Advertising Public Access contact us
 

 
Advanced
Current Issue
First Edition
Future Articles
Archives
Submit to Blood
Search
American Society of Hematology
Meeting Abstracts
Email Alerts
Blood, 15 January 2007, Vol. 109, No. 2, pp. 619-625.
Prepublished online as a Blood First Edition Paper on September 14, 2006; DOI 10.1182/blood-2006-06-027136.


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figure
Right arrow All Versions of this Article:
blood-2006-06-027136v1
109/2/619    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Right arrow Rights and Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhu, J.
Right arrow Articles by Yang, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhu, J.
Right arrow Articles by Yang, Y.
Related Collections
Right arrow Immunobiology
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

arrow to previous article Previous Article  |  Table of Contents  |  Next Article next article arrow

IMMUNOBIOLOGY

Innate immunity against vaccinia virus is mediated by TLR2 and requires TLR-independent production of IFN-ß

Jiangao Zhu1, Jennifer Martinez2, Xiaopei Huang1, and Yiping Yang1,2,

1 Department of Medicine, Division of Medical Oncology, and 2 Department of Immunology, Duke University Medical Center, Durham, NC

Vaccinia virus (VV) has been used extensively as a vaccine vehicle in the clinical application for infectious diseases and cancer. Previous studies have suggested that the unique potency of VV-based vaccine lies in its effective activation of the innate immune system. However, how VV activates innate immune pathways remains largely unknown. In this study, we showed that VV elicited innate immune response through both Toll-like receptor (TLR)–dependent and –independent pathways. The TLR pathway was mediated by TLR2 and MyD88, leading to the production of proinflammatory cytokines, whereas activation of the TLR-independent pathway resulted in the secretion of IFN-ß. More importantly, both TLR-dependent and -independent pathways were required for activating innate and adaptive immunity to VV in vivo. These findings represent the first evidence that innate immune recognition of VV is mediated by TLR2, demonstrate that one pathogen can target both TLR and non-TLR innate immune pathways to work together in achieving efficient activation of host defense, and suggest potential new strategies for the design of effective vaccines.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
J. Immunol.Home page
Y. Zhao, C. De Trez, R. Flynn, C. F. Ware, M. Croft, and S. Salek-Ardakani
The Adaptor Molecule MyD88 Directly Promotes CD8 T Cell Responses to Vaccinia Virus
J. Immunol., May 15, 2009; 182(10): 6278 - 6286.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
X. Ma, A. Serna, R.-H. Xu, and L. J. Sigal
The Amino Acid Sequences Flanking an Antigenic Determinant Can Strongly Affect MHC Class I Cross-Presentation without Altering Direct Presentation
J. Immunol., April 15, 2009; 182(8): 4601 - 4607.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
M. Quigley, J. Martinez, X. Huang, and Y. Yang
A critical role for direct TLR2-MyD88 signaling in CD8 T-cell clonal expansion and memory formation following vaccinia viral infection
Blood, March 5, 2009; 113(10): 2256 - 2264.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
Z. Waibler, M. Anzaghe, T. Frenz, A. Schwantes, C. Pohlmann, H. Ludwig, M. Palomo-Otero, A. Alcami, G. Sutter, and U. Kalinke
Vaccinia Virus-Mediated Inhibition of Type I Interferon Responses Is a Multifactorial Process Involving the Soluble Type I Interferon Receptor B18 and Intracellular Components
J. Virol., February 15, 2009; 83(4): 1563 - 1571.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
M. Quigley, X. Huang, and Y. Yang
STAT1 Signaling in CD8 T Cells Is Required for Their Clonal Expansion and Memory Formation Following Viral Infection In Vivo
J. Immunol., February 15, 2008; 180(4): 2158 - 2164.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
J. Martinez, X. Huang, and Y. Yang
Direct Action of Type I IFN on NK Cells Is Required for Their Activation in Response to Vaccinia Viral Infection In Vivo
J. Immunol., February 1, 2008; 180(3): 1592 - 1597.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
P. Novy, M. Quigley, X. Huang, and Y. Yang
CD4 T Cells Are Required for CD8 T Cell Survival during Both Primary and Memory Recall Responses
J. Immunol., December 15, 2007; 179(12): 8243 - 8251.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
Z. Waibler, M. Anzaghe, H. Ludwig, S. Akira, S. Weiss, G. Sutter, and U. Kalinke
Modified Vaccinia Virus Ankara Induces Toll-Like Receptor-Independent Type I Interferon Responses
J. Virol., November 15, 2007; 81(22): 12102 - 12110.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
Q. Zhang, Y. A. Yu, E. Wang, N. Chen, R. L. Danner, P. J. Munson, F. M. Marincola, and A. A. Szalay
Eradication of Solid Human Breast Tumors in Nude Mice with an Intravenously Injected Light-Emitting Oncolytic Vaccinia Virus
Cancer Res., October 15, 2007; 67(20): 10038 - 10046.
[Abstract] [Full Text] [PDF]


Home page
J. Leukoc. Biol.Home page
S. Chang, A. Dolganiuc, and G. Szabo
Toll-like receptors 1 and 6 are involved in TLR2-mediated macrophage activation by hepatitis C virus core and NS3 proteins
J. Leukoc. Biol., September 1, 2007; 82(3): 479 - 487.
[Abstract] [Full Text] [PDF]



 click for free articles
home about blood authors subscriptions permissions advertising public access contact us
  Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020