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A New Mouse Model That Spontaneously Develops Chronic Liver Inflammation and Fibrosis

Journal article
Authors N. Fransen-Pettersson
N. Duarte
J. Nilsson
M. Lundholm
S. Mayans
A. Larefalk
T. D. Hannibal
L. Hansen
A. Schmidt-Christensen
F. Ivars
Susanna Cardell
R. Palmqvist
B. Rozell
D. Holmberg
Published in Plos One
Volume 11
Issue 7
ISSN 1932-6203
Publication year 2016
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Language en
Keywords primary biliary-cirrhosis, killer t-cells, nonobese diabetic mice, nkt, cells, animal-models, solid-organ, disease, repair, mechanisms, hepatitis, Science & Technology - Other Topics
Subject categories Clinical Medicine


Here we characterize a new animal model that spontaneously develops chronic inflammation and fibrosis in multiple organs, the non-obese diabetic inflammation and fibrosis (N-IF) mouse. In the liver, the N-IF mouse displays inflammation and fibrosis particularly evident around portal tracts and central veins and accompanied with evidence of abnormal intrahepatic bile ducts. The extensive cellular infiltration consists mainly of macrophages, granulocytes, particularly eosinophils, and mast cells. This inflammatory syndrome is mediated by a transgenic population of natural killer T cells (NKT) induced in an immunodeficient NOD genetic background. The disease is transferrable to immunodeficient recipients, while polyclonal T cells from unaffected syngeneic donors can inhibit the disease phenotype. Because of the fibrotic component, early on-set, spontaneous nature and reproducibility, this novel mouse model provides a unique tool to gain further insight into the underlying mechanisms mediating transformation of chronic inflammation into fibrosis and to evaluate intervention protocols for treating conditions of fibrotic disorders.

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