[Exploring the research on the molecular mechanisms of autoimmune liver diseases].

Abstract

Autoimmune liver diseases include subtypes such as autoimmune hepatitis and primary biliary cholangitis, which are caused by abnormal immune system attacks on hepatocytes or bile ducts. This article reviews their molecular mechanisms from three aspects: genetics, environment, and immunity. Human leukocyte antigen (HLA) gene polymorphisms such as DRB10301 and DRB10405 show regional specificity, and non-HLA gene variants such as CTLA4 and FAS also contribute to disease development in terms of genetic factors. Cross-immune responses are triggered through 'molecular mimicry," disturbances in bile acid metabolism and gut microbiota imbalances affect disease progression via the gut-liver axis; and Escherichia coli infection is closely related to primary biliary cholangitis on the basis of environmental factors. Regulatory T cell dysfunction disrupts self-tolerance, abnormal activation of Th17 cells, and alterations in mucosa-associated invariant T cell function lead to liver damage, and chemokines exacerbate local inflammation in terms of immune regulation. The above mechanisms collectively form a molecular network for the pathogenesis of autoimmune liver disease, providing a basis for targeted therapy.