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Related Experiment Video

Updated: Jan 29, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
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Cleavage-Resistant CYLD Protects Against Autoimmune Hepatitis.

Han Liu1, Chen Su2, Jianling Liu1

  • 1CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, P. R. China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 28, 2026
PubMed
Summary

Proteolytic cleavage of cylindromatosis (CYLD) in macrophages drives autoimmune hepatitis progression. Inhibiting MEK1/2 signaling, a key downstream pathway, offers a potential therapeutic strategy for this liver disease.

Keywords:
CYLDMEK1/2autoimmune hepatitisimmune‐mediated hepatitis

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Area of Science:

  • Immunology
  • Hepatology
  • Molecular Biology

Background:

  • Autoimmune hepatitis (AIH) is an immune-mediated liver disease with poorly understood pathogenic mechanisms.
  • AIH can lead to severe liver complications including fibrosis, cirrhosis, and hepatocellular carcinoma.
  • Current therapies for AIH are limited by incomplete understanding of disease drivers.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying autoimmune hepatitis (AIH) progression.
  • To identify novel therapeutic targets for AIH.
  • To investigate the role of cylindromatosis (CYLD) in experimental autoimmune hepatitis (EAH).

Main Methods:

  • Utilized a concanavalin A-induced murine model of experimental autoimmune hepatitis (EAH).
  • Generated and analyzed mice with macrophage-specific, cleavage-resistant Cyld (CyldD215A/D215A) mutation.
  • Investigated the interaction between CYLD, TRIM25, and MEK1/2 signaling pathways in macrophages.
  • Assessed the therapeutic potential of MEK1/2 inhibition in EAH.

Main Results:

  • Proteolytic cleavage of CYLD at Asp215 was identified as a critical event promoting EAH progression.
  • Macrophage-specific CyldD215A/D215A mutant mice showed significant protection from hepatic injury.
  • TNFα-induced CYLD cleavage in macrophages enhances alarmin-triggered chemokine production via MEK1/2 activation.
  • CYLD and TRIM25 cooperatively regulate MEK1/2 ubiquitination, promoting its activation and subsequent chemokine production.
  • Pharmacological MEK1/2 inhibition markedly reduced EAH severity.

Conclusions:

  • A novel CYLD-MEK1/2 signaling axis in macrophages plays a crucial role in orchestrating hepatic inflammation in AIH.
  • CYLD stability is a key regulator of liver inflammation.
  • MEK signaling represents a promising therapeutic target for autoimmune hepatitis.