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Cited by 261

The DOI matches its Crossref record; 118 of the 118 references it cites were found in a registry or an index.

Role of IL-17 and Th17 Cells in Liver Diseases

Open access
Hammerich, Linda, Heymann, Felix, Tacke, Frank·2011·Clinical and Developmental Immunology

Abstract

Unbalanced Th1/Th2 T-cell responses in the liver are a characteristic of hepatic inflammation and subsequent liver fibrosis. The recently discovered Th17 cells, a subtype of CD4+T-helper cells mainly producing IL-17 and IL-22, have initially been linked to host defense against infections and to autoimmunity. Their preferred differentiation upon TGF β and IL-6, two cytokines abundantly present in injured liver, makes a contribution of Th17 cells to hepatic inflammation very likely. Indeed, initial studies in humans revealed activated Th17 cells and Th17-related cytokines in various liver diseases. However, functional experiments in mouse models are not fully conclusive at present, and the pathogenic contribution of Th17 cells to liver inflammation might vary upon the disease etiology, for example, between infectious and autoimmune disorders. Understanding the chemokines and chemokine receptors promoting hepatic Th17 cell recruitment (possibly CCR6 or CCR4) might reveal new therapeutic targets interfering with Th17 migration or differentiation in liver disease.

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Metadata

Authors
Hammerich, L., Heymann, F., & Tacke, F.
Venue
Clinical and Developmental Immunology
Publisher
Wiley
Published
2011
Volume
2011
Pages
1-12
ISSN
  • 1740-2522 (ISSN-L)
  • 1740-2530
OpenAlex
W2083214591
Cited by
261
References
118
FWCI
9.60
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Role of IL-17 and Th17 Cells in Liver Diseases. https://app.cochat.ai/papers/10.1155/2011/345803
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Hammerich, L., Heymann, F., & Tacke, F. (2011). Role of IL-17 and Th17 Cells in Liver Diseases. Clinical and Developmental Immunology. https://doi.org/10.1155/2011/345803

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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