Armed CD4+ Th1 effector cells and activated macrophages participate in bile duct injury in murine biliary atresia.

ABSTRACT: Biliary atresia (BA) is an inflammatory cholangiopathy of infancy. A proposed mechanism regarding the pathogenesis of BA is that of a virus-induced, immune-mediated injury to bile ducts. The rotavirus (RRV)-induced murine model of BA was utilized to determine the hepatic inflammatory response related to ductal obstruction and if the immune response recapitulated human BA. One week after infection, there was a significant increase in liver CD4(+) T cells producing IFN-gamma and in macrophages producing TNF-alpha. The intrahepatic pattern of inflammation evolved rapidly from an initial predominant CD4(+) Th1 cellular response to a subsequent influx of activated macrophages producing TNF-alpha and iNOS. This immune response persisted despite viral clearance and was representative of the hepat

SUBMITTER: Mack CL 

PROVIDER: S-EPMC1950158 | biostudies-literature | 2005 May

REPOSITORIES: biostudies-literature