Treg cells in the course of chronic hepatitis C virus
infection partially normalize in longitudinal
observation after successful DAA treatment
regardless of hepatic fibrosis stage

Zientarska, Agata; Kaczmarek, Mariusz; Mozer‐Lisewska, Iwona; Kowala‐Piaskowska, Arleta; Witkowska, Aleksandra; Zeromski, J

doi:10.5114/ceh.2021.107122

Cited by 3 publications

(3 citation statements)

References 38 publications

(45 reference statements)

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“…Although the percentages of Treg in normal ALT levels were higher than those of the patients with high ALT levels, no statistically significant difference was observed in percentages of Treg between CHC patients with high ALT levels and normal ALT levels (23). Likewise, there was no correlation between APRI and FIB-4 scores and Treg percentages, probably because the AST and platelet values used in this scoring did not deviate much from the normal values due to the relatively mild clinics of the CHC patients included in the study (24).…”

Section: Discussionmentioning

confidence: 78%

Evaluation of Regulatory T Cells in Chronic Hepatitis C Patients

Tok

Şener

Aksoy-Gokmen

et al. 2021

Infect Dis Clin Microbiol

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Background: Although there have been significant improvements in treatment strategies, hepatitis C infection is still among the most critical public health problems worldwide. Upon entry of hepatitis C virus (HCV) into host liver cells, many antagonist immune responses are induced, including the production of regulatory T cells (Tregs). The main function of Tregs is coordinating an appropriate immune response, including suppression of this response once it is no longer needed. Tregs protect cells from immunopathologic damage of HCVspecific T cells but, on the other hand, cause viral persistence, cirrhosis and hepatocellular carcinoma (HCC). In this study, we aimed to determine whether the evaluation of Tregs in hepatitis C patients was a useful method for indicating disease chronicity. Materials and Methods:The peripheral blood samples were taken from sixty volunteers, including 30 non-cirrhotic chronic hepatitis C patients and 30 healthy controls selected from infectious diseases outpatient/clinic service applicants. Their CD4+CD25 high FoxP3+CD152+CD127 low Treg distributions were measured by flow cytometry, using recently identified markers combined.Results: Treg percentages of the subjects with hepatitis C infection (7.97±1.25) were significantly higher than those of the healthy control group (4.29±1.37) (p<0.05). Additionally, the percentages of Tregs were strongly correlated with HCV RNA load (r=0.725, p<0.05) as well as serum AFP levels (r=0.711, p<0.05). Conclusion:Tregs are thought to play an important role in the immunology of HCV infection, thereby providing a promising method for the prediction of disease prognosis and for potentially developing new therapeutic strategies by targeting the Treg.

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Section: Discussionmentioning

confidence: 78%

Evaluation of Regulatory T Cells in Chronic Hepatitis C Patients

Tok

Şener

Aksoy-Gokmen

et al. 2021

Infect Dis Clin Microbiol

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“…However, the effect of CD4 on liver fibrosis appears to be insignificant. For example, while the number of CD4 + T cells is reduced after antiviral therapy, HCV hepatic fibrosis is not alleviated (40). Moreover, there is no significant difference in CD4 + lymphocytes between patients with non-alcoholic hepatic fibrosis and controls (40,41).…”

Section: Results Of the Ppi Network Analysismentioning

confidence: 97%

“…For example, while the number of CD4 + T cells is reduced after antiviral therapy, HCV hepatic fibrosis is not alleviated (40). Moreover, there is no significant difference in CD4 + lymphocytes between patients with non-alcoholic hepatic fibrosis and controls (40,41). The analysis results of a study on CD4 + T lymphocytes and hepatic fibrosis did not comply with the expected assumptions, and no other relevant studies have been conducted; however, this issue is worthy of further in-depth study.…”

Section: Results Of the Ppi Network Analysismentioning

confidence: 99%

Exploration of new therapeutic targets for viral hepatic fibrosis, alcoholic hepatic fibrosis, and non-alcoholic hepatic fibrosis

Wang¹,

Wang²,

Li³

et al. 2022

Ann Transl Med

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Background: Hepatic fibrosis is a widespread disease worldwide. Millions of people lose their lives due to hepatic fibrosis every year. The main causes of hepatic fibrosis include viral infection, alcoholism, and obesity. Many studies have been conducted on the single factors that cause hepatic fibrosis; however, no studies have examined whether hepatic fibrosis caused by multiple factors has concomitant expression molecules and signaling pathways. In this study, we sought to analyze the common differentially expressed messenger ribonucleic acids (mRNAs) of hepatic fibrosis caused by different factors, including hepatitis B virus (HBV) hepatic fibrosis, alcoholic hepatic fibrosis, and non-alcoholic hepatic fibrosis, and identify potential preventive and therapeutic targets.Methods: The GSE171294, GSE142530, and GSE126848 data sets from the Gene Expression Omnibus (GEO) public database were used in this study. A |log fold change| >0.5 and a P value <0.05 were defined as differentially expressed mRNAs via R software screening. To further screen the target mRNAs, the differential mRNAs were subjected to a functional enrichment analysis based on the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Finally, the relationships between differentially expressed mRNA-encoded proteins were analyzed by a protein-protein interaction (PPI) analysis.Results: A total of 54 differentially expressed mRNAs were identified. The KEGG analysis showed that the functions of different mRNAs mainly focused on Gonadotropin Releasing Hormone (GnRH) secretion, bile secretion and insulin secretion. The GO enrichment analysis showed that the differential mRNAs were mainly present in the cytoplasmic membrane region and exerted biological functions, such as activating channels and binding proteins by regulating biological processes (BPs), such as cells, cytoskeleton and heparin. The PPI network analysis revealed 16 nodes with 12 pairs of interactions. The 16 critical nodes included BCL6,

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