ArticleLiver international : official journal of the International Association for the Study of the Liver2009
The role of Ifng in alterations in liver gene expression in a mouse model of fulminant autoimmune hepatitis.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- STAT1 expression in myeloid cells restrains murine norovirus-induced hepatitis and fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Microarray-based transcriptional profiling of a mouse model of autoimmune hepatitis.FEBS open bio · 2020Article
- Sex-Dependent Effects on Liver Inflammation and Gut Microbial Dysbiosis After Continuous Developmental Exposure to Trichloroethylene in Autoimmune-Prone Mice.Frontiers in pharmacology · 2020Article
- Deriving a Boolean dynamics to reveal macrophage activation with in vitro temporal cytokine expression profiles.BMC bioinformatics · 2019Article
- Immunopathogenic Mechanisms of Autoimmune Hepatitis: How Much Do We Know from Animal Models?International journal of molecular sciences · 2016Review
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4Toxicology letters · 2016Article
- Identification of Optimal Mouse Models of Systemic Sclerosis by Interspecies Comparative Genomics.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- Liver inflammation in a mouse model of Th1 hepatitis despite the absence of invariant NKT cells or the Th1 chemokine receptors CXCR3 and CCR5.Laboratory investigation; a journal of technical methods and pathology · 2012Article
- Drug-induced autoimmune-like hepatitis.Digestive diseases and sciences · 2011Review
- Type 1 T helper cells induce the accumulation of myeloid-derived suppressor cells in the inflamed Tgfb1 knockout mouse liver.Hepatology (Baltimore, Md.) · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsBALB/c mice with a homozygous deficiency in the Tgfb1 gene are a model of fulminant autoimmune hepatitis (AIH), spontaneously and rapidly developing Th1-mediated IFN-gamma-dependent necroinflammatory liver disease. We sought to understand the molecular basis for fulminant Th1 liver disease and the specific role of the Ifng gene.
methodsGlobal gene expression in livers from BALB/c Tgfb1(-/-) mice with and without an intact Ifng gene was assessed by microarray analysis. Expression patterns were confirmed by quantitative reverse transcriptase-polymerase chain reaction. Gene ontology clustering analysis was performed to identify altered pathways. The contributions of Ifng to altered expression pathways were quantified.
resultsOver 100 genes were strongly (>10-fold) upregulated, most encoding proteins involved in immune function/response. Chemokines were the most prominently upregulated group, with eight chemokine genes upregulated >10-fold. Ifng was necessary for the upregulation of CXC chemokines gene, but not of CC chemokine genes. By quantitative analysis, Ifng's role in liver gene upregulation varied greatly among overexpressed genes.
conclusionsGene expression changes indicate a particularly important and heretofore unappreciated role for chemokines in fulminant AIH. Ifng has an important role in expression of some but not all genes. Ifng is dichotomous in the regulation of distinct chemokine subfamilies: specifically, Ifng is critical for overexpression of specific CXCL genes but dispensable for overexpression of specific CCL genes. These results provide a clearer understanding of the role of Ifng in the molecular basis of necroinflammatory liver disease.
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