Etiopathogenesis of autoimmune hepatitis

Annarosa Floreani, Paula Restrepo-Jiménez, Maria Francesca Secchi, Sara De Martin, Patrick S Leung, Edward Krawitt, Christopher Bowlus, M. Eric Gershwin, Juan Manuel Anaya

Research output: Contribution to journalReview article

10 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)133-143
Number of pages11
JournalJournal of Autoimmunity
Volume95
DOIs
StatePublished - Dec 1 2018

Fingerprint

Autoimmune Hepatitis
Autoimmunity
Autoantibodies
Liver Diseases
Liver
Hypergammaglobulinemia
Immune Tolerance
Vitamin D Deficiency
Autoantigens
Regulatory T-Lymphocytes
Genetic Predisposition to Disease
Helper-Inducer T-Lymphocytes
Infection
Liver Transplantation
Hepatitis
Single Nucleotide Polymorphism
B-Lymphocytes
Animal Models
Cell Count
Alcohols

Keywords

  • Autoantibodies
  • Autoimmune hepatitis
  • Genome-wide association studies
  • Hormones
  • Microbiome
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Floreani, A., Restrepo-Jiménez, P., Secchi, M. F., De Martin, S., Leung, P. S., Krawitt, E., ... Anaya, J. M. (2018). Etiopathogenesis of autoimmune hepatitis. Journal of Autoimmunity, 95, 133-143. https://doi.org/10.1016/j.jaut.2018.10.020

Etiopathogenesis of autoimmune hepatitis. / Floreani, Annarosa; Restrepo-Jiménez, Paula; Secchi, Maria Francesca; De Martin, Sara; Leung, Patrick S; Krawitt, Edward; Bowlus, Christopher; Gershwin, M. Eric; Anaya, Juan Manuel.

In: Journal of Autoimmunity, Vol. 95, 01.12.2018, p. 133-143.

Research output: Contribution to journalReview article

Floreani, A, Restrepo-Jiménez, P, Secchi, MF, De Martin, S, Leung, PS, Krawitt, E, Bowlus, C, Gershwin, ME & Anaya, JM 2018, 'Etiopathogenesis of autoimmune hepatitis', Journal of Autoimmunity, vol. 95, pp. 133-143. https://doi.org/10.1016/j.jaut.2018.10.020
Floreani A, Restrepo-Jiménez P, Secchi MF, De Martin S, Leung PS, Krawitt E et al. Etiopathogenesis of autoimmune hepatitis. Journal of Autoimmunity. 2018 Dec 1;95:133-143. https://doi.org/10.1016/j.jaut.2018.10.020
Floreani, Annarosa ; Restrepo-Jiménez, Paula ; Secchi, Maria Francesca ; De Martin, Sara ; Leung, Patrick S ; Krawitt, Edward ; Bowlus, Christopher ; Gershwin, M. Eric ; Anaya, Juan Manuel. / Etiopathogenesis of autoimmune hepatitis. In: Journal of Autoimmunity. 2018 ; Vol. 95. pp. 133-143.
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