The potential use of Toll-like receptor agonists to restore the dysfunctional immunity induced by hepatitis C virus

2010 ◽  
Vol 262 (2) ◽  
pp. 96-104 ◽  
Author(s):  
Mohamed L. Salem ◽  
Maha EL-Demellawy ◽  
Abdel Raouf Abou El-Azm
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Toll Like Receptor ◽  
Receptor Agonists ◽  
Potential Use

MicroRNA-155 controls Toll-like receptor 3- and hepatitis C virus-induced immune responses in the liver

2013 ◽  
Vol 21 (2) ◽  
pp. 99-110 ◽  
Author(s):  
M. Jiang ◽  
R. Broering ◽  
M. Trippler ◽  
J. Wu ◽  
E. Zhang ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Toll Like Receptor

253 Hepatitis C virus NS3/4A protein downregulates toll-like receptor 7 signalling pathway

Cytokine ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 299
Author(s):  
Maarit Sillanpää ◽  
Pasi Kaukinen ◽  
Ilkka Julkunen
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Signalling Pathway ◽  
Toll Like Receptor

scholarly journals Toll-Like Receptor 3 Mediates Establishment of an Antiviral State against Hepatitis C Virus in Hepatoma Cells

2009 ◽  
Vol 83 (19) ◽  
pp. 9824-9834 ◽  
Author(s):  
Nan Wang ◽  
Yuqiong Liang ◽  
Santhana Devaraj ◽  
Jie Wang ◽  
Stanley M. Lemon ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatitis Virus ◽  
Hepatoma Cells ◽  
Human Hepatocytes ◽  
Hcv Infection ◽  
Type I Interferons ◽  
Type I ◽  
Toll Like Receptor ◽  
Virus Infections

ABSTRACT Toll-like receptor-3 (TLR3) senses double-stranded RNA, initiating signaling that activates NF-κB and interferon regulatory factor 3 (IRF-3), thereby inducing the synthesis of proinflammatory cytokines, type I interferons, and numerous interferon-stimulated genes (ISGs). This pathway has not been extensively investigated in human hepatocytes, and its role in sensing and protecting against hepatitis virus infections is uncertain. We show here that primary human hepatocytes express TLR3 and robustly upregulate ISGs upon poly(I·C) stimulation. We also show that TLR3 senses hepatitis C virus (HCV) infection when expressed in permissive hepatoma cells, acting independently of retinoic acid-inducible gene I and inducing IRF-3 activation and the synthesis of ISGs that restrict virus replication. In turn, HCV infection reduces the abundance of TRIF, an essential TLR3 adaptor, and impairs poly(I·C)-induced signaling. The induction and disruption of TLR3 signaling by HCV may be important factors in determining the outcome of infection and the ability of HCV to establish persistent infections.

scholarly journals Activation of anti-hepatitis C virus responses via Toll-like receptor 7

2006 ◽  
Vol 103 (6) ◽  
pp. 1828-1833 ◽  
Author(s):  
J. Lee ◽  
C. C. N. Wu ◽  
K. J. Lee ◽  
T.-H. Chuang ◽  
K. Katakura ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Toll Like Receptor

Modulation of Toll like Receptor 3, 7 and 8 Expression in Hepatitis C Virus Infected Patients

2014 ◽  
Vol 4 ◽  
pp. S7
Author(s):  
Rushna Firdaus ◽  
Aritra Biswas ◽  
Kallol Saha ◽  
Anirban Mukherjee ◽  
Sujit Chaudhuri ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Toll Like Receptor

scholarly journals Hepatitis C virus core protein induces fibrogenic actions of hepatic stellate cells via toll-like receptor 2

2011 ◽  
Vol 91 (9) ◽  
pp. 1375-1382 ◽  
Author(s):  
Martin Coenen ◽  
Hans Dieter Nischalke ◽  
Benjamin Krämer ◽  
Bettina Langhans ◽  
Andreas Glässner ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatic Stellate Cells ◽  
Core Protein ◽  
Stellate Cells ◽  
Toll Like Receptor ◽  
Virus Core ◽  
Toll Like Receptor 2
Sign in / Sign up

Export Citation Format

Share Document