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Etiopathogenesis of autoimmune hepatitis

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Floreani A.
Restrepo-Jiménez P.
Secchi M.F.
De Martin S.
Leung P.S.C.
Krawitt E.
Bowlus C.L.
Gershwin M.E.
Anaya, Juan-Manuel

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2018

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Academic Press

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Abstract
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
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Autoantibody , autoimmune , regulatory , helper-inducer , biliary , 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 , Hepatitis , Hla antigens , Humans , Liver , Liver cirrhosis , Liver transplantation , Sex factors , T-lymphocytes , T-lymphocytes , Vitamin d deficiency , Autoantibodies , Autoimmune hepatitis , Genome-wide association studies , Hormones , Microbiome , Primary biliary cholangitis , Primary sclerosing cholangitis
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