scholarly journals Reduced Expression of Toll-Like Receptor 2 on Peripheral Monocytes in Patients with Chronic Hepatitis B

2006 ◽  
Vol 13 (8) ◽  
pp. 972-974 ◽  
Author(s):  
Stephen M. Riordan ◽  
Narelle Skinner ◽  
Jelica Kurtovic ◽  
Stephen Locarnini ◽  
Kumar Visvanathan

ABSTRACT Persistent infection with hepatitis B virus (HBV) likely depends on viral inhibition of host defenses. We report that chronic hepatitis B e antigen-positive HBV infection is associated with a significant reduction in peripheral blood monocyte expression of Toll-like receptor 2, a key component of innate immunity, thereby providing a mechanism by which wild-type HBV may establish persistent infection.

Hepatology ◽  
2006 ◽  
Vol 45 (1) ◽  
pp. 102-110 ◽  
Author(s):  
Kumar Visvanathan ◽  
Narelle A. Skinner ◽  
Alex J.V. Thompson ◽  
Stephen M. Riordan ◽  
Vitini Sozzi ◽  
...  

2018 ◽  
Vol 255 ◽  
pp. 165-170 ◽  
Author(s):  
Quan Zhang ◽  
Junhao Chen ◽  
Mingjie Pan ◽  
Jingli Liu ◽  
Tingting Liu ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Malihe Moradzadeh ◽  
Sirous Tayebi ◽  
Hossein Poustchi ◽  
Kourosh Sayehmiri ◽  
Parisa Shahnazari ◽  
...  

Recognition mechanisms of innate immune response help to improve immunotherapeutic strategies in HBeAg-negative chronic hepatitis B (CHB). Toll-like receptor 2 (TLR2) is an important component of innate immunity. In this study, the frequency of precore mutations of the hepatitis B virus (HBV) and serum TLR2 were evaluated in CHB patients. Fifty-one patients with chronic hepatitis B, negative for HBeAg and detectable HBV DNA, were examined for the presence of mutations in pre-core region of HBV genome by direct sequencing. Serum TLR2 was measured by enzyme-linked immunosorbent assay. Interactions of truncated HBeAg and TLR2 proteins were evaluated with molecular docking software. The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8±2.9 versus 3.4±2.2 ng/mL,P=0.03). There was also a significant correlation between serum ALT and TLR-2 (r=0.46;P=0.01). Docking results illustrated residues within the N-terminus of truncated HBeAg and TLR2, which might facilitate the interaction of these proteins. These findings showed the dominance of G1896A pre-core mutation of HBV variants in this community which was correlated with serum TLR2. Moreover TLR2 is critical for induction of inflammatory cytokines and therefore ALT elevation.


2016 ◽  
Vol 62 (7) ◽  
pp. 617-622 ◽  
Author(s):  
Emine Firat Goktas ◽  
Cemal Bulut ◽  
Mustafa Tugrul Goktas ◽  
Erdem Kamil Ozer ◽  
Ragip Ozgur Karaca ◽  
...  

The immunopathogenesis of chronic hepatitis B (CHB) has not been clarified yet. Toll-like receptors (TLR) are a receptor family that initiates immunity with exogenous–endogenous ligands and plays a role in the pathogenesis of infections. In this study, we aimed to investigate the frequency of TLR 3 1377C/T (rs3775290) polymorphism and its role in patients with CHB. We included 50 healthy individuals as control group and 73 active and 43 inactive hepatitis B patients. All DNA samples were isolated from blood samples. For the detection of TLR 3 1377C/T single-nucleotide polymorphism, restriction fragment length polymorphism was used. A statistically significant difference was determined in Hepatitis B virus (HBV) DNA levels of CHB patients with the CC, CT, and TT genotypes (p = 0.013). The highest levels of HBV DNA were detected in individuals with TT genotypes. Additionally, the frequency of CC genotype was higher in the active CHB patients compared with that of the inactive CHB patients (p = 0.044). No statistically significant difference in TLR 3 1377C/T polymorphism was detected between healthy controls and the hepatitis B patients (p = 0.342). In conclusion, HBV DNA level was higher in the individuals with TT genotype, and CC genotype was more frequent in the active CHB patients. These results suggest a possible association between CHB and TLR 3 gene (1377C/T) polymorphism.


2015 ◽  
Vol 63 (2) ◽  
pp. 320-328 ◽  
Author(s):  
Edward J. Gane ◽  
Young-Suk Lim ◽  
Stuart C. Gordon ◽  
Kumar Visvanathan ◽  
Eric Sicard ◽  
...  

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