[Expression of Toll-like receptor 3 on peripheral blood dendritic cells in HBeAg positive patients with chronic hepatitis B]
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Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix
Published on: October 20, 2021
Bao-yan An1, Qing Xie, Lan-yi Lin
1Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Insights
Toll-like receptor 3 (TLR3) and CD86 expression are altered in chronic Hepatitis B virus (HBV) infection. These immune cell changes suggest a link between abnormal TLR3 and CD86 expression and persistent HBV infection.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Dendritic cells (DCs) play a crucial role in initiating immune responses.
- Toll-like receptor 3 (TLR3) is involved in recognizing viral RNA and activating immune cells.
- Hepatitis B virus (HBV) infection can lead to chronic inflammation and liver disease.
Purpose of the Study:
- To investigate the expression and function of TLR3 on dendritic cells (DCs) in patients with chronic HBV infection.
- To compare TLR3 and co-stimulatory molecule CD86 expression in DCs from healthy volunteers and HBV-infected patients.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) were isolated from healthy volunteers (HV) and chronically HBV-infected patients (CH).
- Dendritic cells (DCs) were cultured and stimulated with poly I:C (a TLR3 agonist).
- Expression levels of TLR3, HLA-DR, CD86, and CD1a were analyzed using flow cytometry and real-time PCR.
Main Results:
- TLR3 expression was upregulated by poly I:C stimulation in both groups, but the increase was slower in the CH group.
- CD86 expression significantly increased in HV after stimulation, while only a slight increase was observed in the CH group.
- No significant differences in HLA-DR and CD1a expression were found between the groups.
Conclusions:
- The delayed upregulation of TLR3 and blunted CD86 response in DCs from CH patients suggest impaired immune activation.
- Abnormal expression patterns of TLR3 and CD86 may contribute to the persistence of HBV infection.
- These findings highlight potential therapeutic targets for managing chronic HBV.
Objective:
To elucidate the roles of Toll-like receptor 3 (TLR3) on dendritic cells (DCs) in HBV infection.
Methods:
Peripheral blood mononuclear cells (PBMCs) were isolated from 48 healthy volunteers (HV) and 50 chronically HBV-infected patients (CH). DCs were induced and proliferated in a culture medium with rhGM-CSF and rhIL-4. We stimulated DCs with poly I:C and then TLR3, HLA-DR, and CD86, and CD1a expressions were examined by flow cytometry at 0 h, 12 h, 24 h and 48 h. The mRNA expressions of TLR3 were quantified by real-time PCR.
Results:
TLR3 expression on DCs before the poly I:C stimulation and afterwards on the 12 h, 24 h, and 48 h were 69.2%+/-20.4%, 76.0%+/-18.6%, 78.2%+/-19.5% and 85.5%+/-6.9% respectively in the CH group, and 70.8%+/-11.2%, 67.5%+/-20.9%, 86.3%+/-14.7%, 68.6%+/-16.9% in the HV group. The expressions of TLR3 were up-regulated significantly at 24 h and 48 h after stimulation with poly I:C in the HV group, and in the CH group they were not significantly increased at 24 h but obviously increased at 48 h. The mRNA expressions of TLR3 increased significantly at 12 h in the HV groups, and at 48 h in CH group. The rate of CD86 expressions increased after poly I:C stimulation, and the increased rates were 12.6%+/-9.8%, 23.8%+/-20.0%, 20.7%+/-14.3% in the CH group, and 31.0%+/-25.0%, 43.4%+/-24.7%, 44.6%+/-25.5% in the HV group at 12 h, 24 h and 48 h after poly I:C stimulation. There was a marked increase of the expression level of CD86 in the HV group. In contrast, the level was only slightly increased in the CH group (31.0% vs 12.6%). The differences between the two groups were significant at 24 h and 48 h. No significant differences were detected in HLA-DR and CD1a between the two groups.
Conclusions:
The increase of expression level of TLR3 is slower in the CH group than that in the HV group. A marked increase of the expression level of CD86 is observed in the HV group. Our results suggest that abnormal expression of TLR3 and CD86 may relate to the persistence of HBV infection.
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