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Aryl hydrocarbon receptor plays protective roles in ConA-induced hepatic injury by both suppressing IFN-γ expression

Hiromi Abe1, Akihiro Kimura, Sanae Tsuruta

  • 1Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan.

International Immunology
|October 24, 2013
PubMed

Insights

The aryl hydrocarbon receptor (AhR) protects against ConA-induced liver injury by boosting IL-22 from innate lymphoid cells and reducing IFN-γ from NKT cells. AhR deficiency increases liver injury sensitivity.

Area of Science:

  • Immunology
  • Hepatology
  • Toxicology

Background:

  • The aryl hydrocarbon receptor (AhR) is a transcription factor involved in environmental pollutant toxicity and tissue injury protection.
  • Concanavalin A (ConA)-induced hepatitis serves as a mouse model for acute liver injury.

Purpose of the Study:

  • To investigate the role of AhR in ConA-induced hepatitis.
  • To elucidate the mechanisms by which AhR influences liver injury.

Main Methods:

  • Utilized a ConA-induced hepatitis mouse model.
  • Employed Ahr (-/-) mice and bone marrow chimera experiments.
  • Analyzed cytokine expression (IFN-γ, IL-22) and cell populations (NKT cells, ILCs).

Main Results:

  • AhR is upregulated during ConA-induced hepatitis, and Ahr (-/-) mice show increased sensitivity.
  • Hematopoietic cells lacking AhR are responsible for hypersensitivity.
  • AhR deficiency leads to increased IFN-γ from NKT cells and decreased IL-22 from ILCs.

Conclusions:

  • AhR plays a critical protective role in ConA-induced liver injury.
  • AhR promotes IL-22 production from ILCs and suppresses IFN-γ from NKT cells, thereby mitigating liver damage.
Keywords:
AhRIFN-γIL-22hepatitisinnate lymphoid cells

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