The interplay of type I and type II interferons in murine autoimmune cholangitis as a basis for sex-biased autoimmunity.

ABSTRACT: We have reported on a murine model of autoimmune cholangitis, generated by altering the AU-rich element (ARE) by deletion of the interferon gamma (IFN-γ) 3' untranslated region (coined ARE-Del^-/- ), that has striking similarities to human primary biliary cholangitis (PBC) with female predominance. Previously, we suggested that the sex bias of autoimmune cholangitis was secondary to intense and sustained type I and II IFN signaling. Based on this thesis, and to define the mechanisms that lead to portal inflammation, we specifically addressed the hypothesis that type I IFNs are the driver of this disease. To accomplish these goals, we crossed ARE-Del^-/- mice with IFN type I receptor alpha chain (Ifnar1) knockout mice. We report herein that loss of type I IFN receptor si

SUBMITTER: Bae HR 

PROVIDER: S-EPMC5856578 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature