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J Hepatol. 2004 Mar;40(3):446-53.

Induction of Mx-2 in rat liver by toxic injury.

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Division of Gastroenterology and Endocrinology, Department of Medicine, Georg-August-University Göttingen, Robert-Koch-Strasse 40, Göttingen 37075, Germany.



Mx proteins are supposed to be strictly regulated by viruses or interferon-alpha (IFN-alpha). We used a non-viral model of acute liver injury to study Mx expression.


We induced toxic liver injury by CCl(4), and studied the expression of IFN-alpha, IFN-gamma, and IFN-inducible antiviral genes (Mx-2; 2'-5' oligoadenylate synthetase, 2-5 A; double-stranded RNA-activated protein kinase, PKR).


Similar to 2-5 A and PKR, Mx-2 gene expression was biphasically induced after CCl(4) administration with a maximum at 24 h, and a second peak at 72 h. On protein level, Mx-2 only was up-regulated. IFN-alpha remained constant for the first 24 h while IFN-gamma peaked at 6 h. Thereafter, IFN-alpha increased to a maximum at 72 h while IFN-gamma decreased to 77+/-4%. Small monocyte-like liver macrophages, but not large macrophages, expressed Mx-2 constitutively. In vitro, IFN-alpha but not IFN-gamma induced Mx-2 in different liver cell populations. IFN-gamma, instead, reduced the susceptibility of liver macrophages to the actions of IFN-alpha.


Our data suggest that Mx expression does not invariably result from the presence of a viral particle or IFN-alpha synthesis but may represent an innate defensive armamentarium that may be up-regulated without antigen specificity upon liver injury.

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