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Updated: Mar 15, 2026

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

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Mincle Signaling Promotes Con A Hepatitis.

Stephanie H Greco¹, Alejandro Torres-Hernandez¹, Aleksandr Kalabin¹

¹S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, New York, NY 10016;

Journal of Immunology (Baltimore, Md. : 1950)

|August 26, 2016

Summary

This study reveals Mincle (Macrophage-inducible C-type lectin) drives T cell-mediated liver injury in Con A hepatitis. Blocking Mincle protects against this sterile inflammation, highlighting its potential therapeutic role.

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Area of Science:

Immunology
Hepatology
Inflammation Research

Background:

Concanavalin A (Con A) hepatitis serves as a T cell-mediated acute liver injury model.
The C-type lectin receptor Mincle's role in non-pathogen-mediated inflammation is unclear.
Mincle's interaction with SAP130 suggests a potential role in Con A hepatitis.

Purpose of the Study:

To investigate the role of Mincle signaling in Con A hepatitis.
To determine if Mincle blockade can ameliorate liver injury.
To elucidate the downstream signaling pathways involved.

Main Methods:

Utilized a murine Con A hepatitis model with wild-type, Mincle(-/-), and Dectin-1(-/-) mice.
Assessed liver injury and inflammatory cell infiltration.
Employed selective inhibitors for C/EBPβ and hypoxia-inducible factor-1α (HIF-1α) signaling.
Conducted bone marrow chimeric and adoptive transfer experiments.

Main Results:

Mincle expression was elevated in hepatic inflammatory cells and endothelial cells in mice and humans.
Mincle deletion or blockade significantly protected against Con A-induced liver injury.
Mincle signaling in myeloid cells was critical for disease pathogenesis.
Mincle blockade reduced C/EBPβ and HIF-1α signaling, lowering nitrite production.

Conclusions:

Mincle acts as a key innate immune driver in Con A hepatitis.
Targeting Mincle signaling offers a potential therapeutic strategy for sterile inflammatory liver diseases.
This study expands the understanding of Mincle's function beyond pathogen recognition.