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Updated: Jan 29, 2026

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IL-11 prevents IFN-γ-induced hepatocyte death through selective downregulation of IFN-γ/STAT1 signaling and ROS

Akimitsu Miyawaki1, Yoshiko Iizuka1, Hitomi Sugino1

  • 1Department of Pharmaceutical Sciences, Musashino University, Tokyo, Japan.

Plos One
|February 20, 2019
PubMed
Abstract

Insights

Interleukin-11 (IL-11) pretreatment protects liver cells from Interferon-gamma (IFN-γ)-induced death by suppressing STAT1 signaling and reducing oxidative stress. This study uncovers mechanisms of selective negative feedback in hepatocyte signaling.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Immunology

Background:

  • Interferon-gamma (IFN-γ) induces liver toxicity via STAT1 activation.
  • Interleukin-11 (IL-11) offers tissue protection through STAT3 activation.
  • Understanding the interplay between these cytokines is crucial for liver health.

Purpose of the Study:

  • To investigate how IL-11 pretreatment protects hepatocytes from IFN-γ-induced cell death.
  • To elucidate the molecular mechanisms, focusing on signal crosstalk.
  • To explore the role of STAT signaling pathways.

Main Methods:

  • Primary mouse hepatocytes were pretreated with IL-11 before IFN-γ exposure.
  • Cell death was assessed by lactate dehydrogenase release.
  • STAT1 and STAT3 activation, and downstream gene expression were analyzed.
  • Oxidative stress markers and ROS scavengers were evaluated.

Main Results:

  • IL-11 pretreatment significantly reduced IFN-γ-induced hepatocyte death.
  • IL-11 attenuated IFN-γ-induced STAT1 activation and downstream pro-death gene expression.
  • IL-11 pretreatment increased ROS scavengers, mitigating oxidative stress.
  • IFN-γ did not inhibit IL-11-induced STAT3 activation.

Conclusions:

  • IL-11 protects hepatocytes from IFN-γ toxicity by suppressing STAT1 signaling and enhancing antioxidant defenses.
  • The findings highlight selective negative feedback mechanisms in cytokine signaling.
  • Further research into these pathways could offer novel therapeutic strategies for liver diseases.

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