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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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Interleukin-17 in Liver Disease Pathogenesis.

Na Li1,2,3, Gen Yamamoto2,3, Hiroaki Fuji2,3

  • 1Shanghai University of Medicine & Health Sciences, Shanghai, P.R. China.

Seminars in Liver Disease
|June 15, 2021
PubMed
Summary

T helper 17 (Th17) cells and Interleukin 17A (IL-17A) signaling are crucial in liver injury, particularly in nonalcoholic steatohepatitis (NASH) and alcohol-associated liver disease (AALD). This review explores the IL-17A-IL-17RA axis role in metabolic liver disease and hepatocellular carcinoma (HCC).

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Area of Science:

  • Immunology
  • Hepatology
  • Cell Biology

Background:

  • T helper 17 (Th17) cells produce Interleukin 17A (IL-17A), vital for pathogen defense.
  • Th17 cell differentiation is influenced by TGF-β1 and IL-6, cytokines also implicated in liver fibrosis.
  • IL-17A exerts its function via the IL-17RA receptor, whose expression is elevated in various liver diseases.

Purpose of the Study:

  • To review the role of IL-17 signaling in metabolic liver injury and hepatocellular carcinoma (HCC).
  • To discuss the involvement of the IL-17A-IL-17RA axis in liver diseases like nonalcoholic steatohepatitis (NASH) and alcohol-associated liver disease (AALD).

Main Methods:

  • Literature review focusing on IL-17 signaling in liver disease pathogenesis.
  • Analysis of the IL-17A-IL-17RA axis in metabolic liver injury and HCC.
  • Discussion of cellular crosstalk in liver injury mediated by IL-17A.

Main Results:

  • IL-17RA expression is upregulated in HBV/HCV infections, NASH, AALD, and HCC.
  • IL-17 signaling contributes to the pathogenesis of metabolic liver injury and HCC.
  • The IL-17A-IL-17RA axis mediates crosstalk between hepatic immune and structural cells.

Conclusions:

  • The IL-17A-IL-17RA axis is a significant factor in the development and progression of metabolic liver diseases and HCC.
  • Understanding this axis offers potential therapeutic targets for liver conditions.
  • IL-17 signaling impacts hepatic macrophages, hepatocytes, and myofibroblasts in liver injury.