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Updated: Jun 13, 2026

Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice

Induction of an Inflammatory Response in Primary Hepatocyte Cultures from Mice

Published on: March 10, 2017

Tolerance induction in response to liver inflammation.

Annette Erhardt¹, Gisa Tiegs

¹Institute of Experimental Immunology and Hepatology, Center of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Digestive Diseases (Basel, Switzerland)

|May 13, 2010

Summary

Liver inflammation tolerance develops via regulatory T cells producing IL-10. This immune tolerance is dependent on specific chemokine receptors, highlighting a mechanism for controlling liver injury.

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Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms

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Published on: May 29, 2020

Area of Science:

Immunology
Hepatology
Inflammation Research

Background:

The liver's unique anatomical position necessitates mechanisms to balance immune tolerance to gut antigens and responses to pathogens.
Immune-mediated liver injury models are crucial for understanding hepatic immune regulation.

Purpose of the Study:

To investigate the mechanisms of immune tolerance induction following liver inflammation in a murine model.
To elucidate the role of regulatory T cells and specific chemokine receptors in resolving Concanavalin A (ConA)-induced hepatitis.

Main Methods:

Induction of liver damage using Concanavalin A (ConA) in mice.
Measurement of plasma and liver cytokine levels.
Flow cytometry analysis of intrahepatic and splenic immune cell subsets.
Assessment of regulatory T cell function in vitro and in vivo.

Main Results:

ConA hepatitis involves CD4+ T cells, NKT cells, and Kupffer cells releasing IFN-gamma and TNF-alpha.
Tolerance to ConA rechallenge developed within 8 days, characterized by reduced liver enzymes, decreased Th1/Th17 responses, and increased IL-10 production.
IL-10 was produced by CD4+CD25+FoxP3+ regulatory T cells and Kupffer cells; these regulatory T cells showed enhanced immunosuppressive capacity.
Hepatitis severity was increased in mice lacking CCR5 or CXCR3 chemokine receptors.

Conclusions:

ConA-induced liver tolerance is mediated by IL-10-producing regulatory T cells.
The trafficking of these regulatory T cells into the liver appears to be dependent on IFN-gamma-inducible chemokine receptors CCR5 and CXCR3.