Journal List > J Bacteriol Virol > v.45(4) > 1034199

Shin, Lee, and Cho: Role of Th17 and Treg during the Chronic Infection of Hepatitis C Virus

Abstract

Hepatitis C virus (HCV) is one of the main causes of liver disease. 1~2% of the Korean people has been reported to be infected by HCV. Although HCV is less infectious than hepatitis B virus (HBV), it is more prone to develop chronic infection (~ 80%) which may link to cirrhosis and hepatocellular carcinogenesis. In addition, prevalence of hepatitis caused by HCV infection is gradually increased every year in Korea. Recently, a large number of clinical trials using direct-acting antiviral (DAA) drugs have been shown efficient therapeutic results for chronic HCV infections and some of them are on the market. However, there is still a concern on viral evasion to the DAAs and the effective mechanisms of immunological clearance of HCV remains to be elucidated. Here, we introduce the recent findings on the role of Th17-Treg axis which may play a critical role of the viral pathogenesis and/or immunological defense against HCV infection. The underlying regulatory mechanisms of Th17-Treg axis might be a potential candidate for the better control of HCV chronic infections.

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Figure 1.
Subsets of immune cells producing IL-17 and their targets. There are three major subsets of IL-17-producing cells; T helper 17(Th17), RORγt+ innate lymphoid cells (IL-17+ ILC3) and gamma-delta T cells (γδ T cells). IL-17 produced from these cells contributes to inflammation by increasing production of inflammatory cytokines from the target cells, such as epithelial cells, fibroblasts, macrophages, dendritic cells, and endothelial cells. CCL20, chemokine CC motif ligand 20; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage CSF.
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