Etiopathogenesis of autoimmune hepatitis

Autoimmune hepatitis is a chronic inflammatory liver disease characterized by hypergammaglobulinemia, the presence of autoantibodies, and inflammation within the liver, including lymphocytic infiltrates and interface hepatitis. Autoimmune hepatitis shows a female predominance and can present at any age and in any ethnicity. The disease is thought to be a consequence of a break of immune tolerance leading to an autoimmune process that induces liver injury. The self-attack is triggered by T-helper cell-mediated liver autoantigen recognition and B-cell production of autoantibodies, and is sustained by impaired regulatory T cells number and function. Superimposed on a genetic predisposition, infections and environmental factors have been studied as triggering factors for the disease. Allelic variants in the HLA locus have been associated with susceptibility; associations with single nucleotide polymorphisms within non-HLA genes have also been assessed. Several factors have been described as triggers of autoimmune responses in predisposed individuals, including infections, alcohol, vitamin D deficiency, and an altered composition of the intestinal microbiome. Importantly, drugs and herbal agents may trigger classical autoimmune hepatitis, or may induce a liver disease with autoimmune features. Interactions between female hormones and genetic factors have been hypothesized to play a role in autoimmunity, although the exact role for these factors has not been fully established. Herein we present a review of the etiology of autoimmune hepatitis including de novo autoimmune hepatitis post-liver transplantation as well as animal models for its study. © 2018

• Fecha de publicación: 2018
• Institución: Universidad del Rosario
• Repositorio: Repositorio EdocUR - U. Rosario
• Idioma: eng
• OAI Identifier: oai:repository.urosario.edu.co:10336/22262
• Acceso en línea: https://doi.org/10.1016/j.jaut.2018.10.020; https://repository.urosario.edu.co/handle/10336/22262
• Palabra clave: Autoantibody; Autoantigen; Cytochrome p450 1a2; Cytochrome p450 2a6; Drug; Herbaceous agent; Sex hormone; Hla antigen; Alcohol consumption; Alcohol metabolism; Autoimmune hepatitis; Autoimmunity; B lymphocyte; Bacterial infection; Environmental factor; Genetic predisposition; Genetic susceptibility; Helper cell; Heredity; Histocompatibility gene; Human; Immunization; Immunological tolerance; Immunopathogenesis; Intestine flora; Knockout mouse; Liver homogenate; Liver injury; Liver transplantation; Molecular mimicry; Mouse model; Nonhuman; Parasitosis; Postoperative complication; Priority journal; Regulatory t lymphocyte; Review; Single nucleotide polymorphism; Toxic hepatitis; Transgenic mouse; Virus infection; Vitamin d deficiency; Adverse event; Alcoholism; Animal; Autoimmune hepatitis; Biliary cirrhosis; Biosynthesis; Communicable disease; Complication; Genetics; Genotype environment interaction; Immunology; Liver; Pathology; Sex factor; Vitamin d deficiency; Alcoholism; Animals; Autoantibodies; Autoantigens; B-lymphocytes; Communicable diseases; Gene-environment interaction; Genetic predisposition to disease; Hla antigens; Humans; Liver; Liver transplantation; Sex factors; Vitamin d deficiency; Autoantibodies; Autoimmune hepatitis; Genome-wide association studies; Hormones; Microbiome; Primary biliary cholangitis; Primary sclerosing cholangitis; autoimmune; regulatory; helper-inducer; biliary; Hepatitis; Liver cirrhosis; T-lymphocytes; T-lymphocytes
• License: Abierto (Texto Completo)