Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

T cell immunity in autoimmune hepatitis.

Yasunori Ichiki1, Christopher A Aoki, Christopher L Bowlus

  • 1Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, TB192, One Shields Avenue, Davis, CA 95616, USA.

Autoimmunity Reviews
|July 2, 2005
PubMed
Summary

T cells, including CD4+, CD8+, and gammadelta T cells, are central to autoimmune hepatitis (AIH) pathogenesis. Genetic factors and potential molecular mimicry likely trigger the immune response, leading to liver damage.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Long-Term Safety and Efficacy of Obeticholic Acid in Patients With Primary Biliary Cholangitis: Final Results of the POISE Long-Term Safety Extension.

Alimentary pharmacology & therapeutics·2026
Same author

Evolving Concepts of Treatment Targets for Primary Biliary Cholangitis: A Global Perspective.

The American journal of gastroenterology·2026
Same author

Author Response to "Comment on Prediagnosis Alkaline Phosphatase and Antimitochondrial Antibody Positivity Vary by Race/Ethnicity Among Patients With Primary Biliary Cholangitis".

Journal of gastroenterology and hepatology·2026
Same author

Seladelpar in patients with primary biliary cholangitis and compensated cirrhosis: Efficacy and safety from RESPONSE and ASSURE studies.

Hepatology communications·2026
Same author

Gaps in Guideline Adherence for Primary Sclerosing Cholangitis in North America-A 5-Year Analysis.

Liver international : official journal of the International Association for the Study of the Liver·2026
Same author

Clover Honey Limits Survival of Enterotoxigenic Escherichia coli in an In Vitro Gastric Model and Reduces In Vitro Fermentation pH of Small Intestine Microbes.

The Journal of nutrition·2026

Area of Science:

  • Immunology
  • Hepatology
  • Autoimmunity

Background:

  • Autoimmune hepatitis (AIH) pathogenesis involves T cell-mediated immune responses.
  • While CD4+ T cells were initially considered primary drivers, emerging evidence highlights significant roles for CD8+ and gammadelta T cells.
  • Genetic predispositions (HLA genotypes) and T cell receptor clonal expansion suggest antigen-specific triggers.

Purpose of the Study:

  • To elucidate the multifaceted role of various T cell subsets in autoimmune hepatitis (AIH).
  • To explore potential triggers and mechanisms initiating the autoimmune response in AIH.
  • To understand the sequence of events leading to liver injury in AIH.

Main Methods:

  • Review of existing literature on T cell subsets in AIH.

Related Experiment Videos

  • Analysis of genetic associations (HLA genotypes) and T cell receptor repertoire in AIH patients.
  • Examination of proposed mechanisms involving viral hepatitis, molecular mimicry, and impaired immune regulation.
  • Main Results:

    • CD8+ and gammadelta T cells, in addition to CD4+ T cells, are implicated in AIH immunopathogenesis.
    • Self-antigens or molecular mimics, potentially triggered by viral infections, are proposed initiators of the immune response.
    • Impaired regulatory T cells and defective apoptosis may exacerbate T cell activation and clonal expansion.

    Conclusions:

    • T cells orchestrate the autoimmune attack in AIH through diverse mechanisms.
    • The initiation of AIH involves a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation.
    • Ultimately, T cell activation leads to autoantibody production, cytokine release, and hepatocyte cytotoxicity, driving liver disease progression.