ArticleHepatology (Baltimore, Md.)2013
Hepatitis C virus promotes T-helper (Th)17 responses through thymic stromal lymphopoietin production by infected hepatocytes.
Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 54 citations in OpenAlex.
- Divergent Inflammatory Profiles but No Predictive Biomarkers of Psychiatric Sequelae After Viral Infection: A 12-Month Cohort Study.International journal of molecular sciences · 2026Article
- Validation of signature molecular profiles of advanced HCV liver disease in hepatocellular carcinoma patients.Virus research · 2025Article
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
- Role of the type 3 cytokines IL-17 and IL-22 in modulating metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Review
- Role of thymic stromal lymphopoietin in allergy and beyond.Nature reviews. Immunology · 2023Review
- Single-cell atlas of hepatic T cells reveals expansion of liver-resident naive-like CD4Journal of hepatology · 2021Article
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- TSLP induces a proinflammatory phenotype in circulating innate cells and predicts prognosis in sepsis patients.FEBS open bio · 2019Article
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- TSLP Exacerbates Septic Inflammation via Murine Double Minute 2 (MDM2) Signaling Pathway.Journal of clinical medicine · 2019Article
- Review
- Review
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- Epidemiological Profile and Risk Factors for Acquiring HBV and/or HCV in HIV-Infected Population Groups in Nepal.BioMed research international · 2018Article
- Molecular basis of hepatocellular carcinoma induced by hepatitis C virus infection.World journal of hepatology · 2017Review
- The proportion of different interleukin-17-producing T-cell subsets is associated with liver fibrosis in chronic hepatitis C.Immunology · 2017Article
- Immunity and Fibrogenesis: The Role of Th17/IL-17 Axis in HBV and HCV-induced Chronic Hepatitis and Progression to Cirrhosis.Frontiers in immunology · 2017Review
- Article
- Hepatic fibrosis and immune phenotype vary by HCV viremia in HCV/HIV co-infected subjects: A Women's interagency HIV study.Medicine · 2016Article
- Immune responses and immunopathology in acute and chronic viral hepatitis.Nature reviews. Immunology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
unlabelledHepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma. Here we report that infection of hepatic cells by HCV stimulates nuclear factor kappa B (NFκB)-dependent production of thymic stromal lymphopoietin (TSLP). Hepatocyte-derived TSLP in turn conditions dendritic cells (DCs) to drive T-helper (Th)17 differentiation. The TSLP secreted by HCV-infected hepatoma cells is capable of activating human monocyte-derived DCs by up-regulating the expression of CD40, CD86, CCL17, CCL22, and CCL20 which are activating markers of DCs. In addition, the production of key cytokines for Th17 differentiation, transforming growth factor beta (TGF-β), interleukin (IL)-6, and IL-21, is enhanced by human monocytes upon coculture with HCV-infected cells. Importantly, the blockade of TSLP using neutralizing antibody prevented the activation and maturation of DCs as well as the production of Th17 differentiation cytokines. DC conditioning by TSLP secreted from HCV-infected cells activated naïve CD4+ T lymphocytes, resulting in Th17 differentiation. Furthermore, we can detect substantial levels of hepatocyte TSLP in fibrotic liver tissue from chronic HCV patients. Thus, blockade of TSLP released by HCV-infected hepatocytes may suppress the induction/maintenance of hepatic Th17 responses and halt the progression of chronic liver disease to fibrosis and liver failure.
conclusionHepatocyte-derived TSLP conditions DCs to drive Th17 differentiation. Treatment of TSLP neutralizing antibody in HCV-infected hepatocyte/DC coculture abrogates DC conditioning and thereby inhibits Th17 differentiation.
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