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Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

Overview
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...

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Related Experiment Video

Updated: Jun 13, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
09:03

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Published on: February 3, 2012

Adaptive immunity in autoimmune hepatitis.

Maria Serena Longhi1, Yun Ma, Giorgina Mieli-Vergani

  • 1Institute of Liver Studies, King's College London School of Medicine at King's College Hospital, London, UK.

Digestive Diseases (Basel, Switzerland)
|May 13, 2010
PubMed
Summary
This summary is machine-generated.

Autoimmune hepatitis (AIH) involves an immune attack on the liver, driven by T helper cells. Impaired regulatory T cells allow persistent liver damage in AIH.

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Area of Science:

  • Immunology
  • Hepatology
  • Autoimmunity

Background:

  • Interface hepatitis lesions suggest autoimmune attack in autoimmune hepatitis (AIH).
  • Immunohistochemistry reveals predominant alphabeta T cells, including CD4+ helper and CD8+ cytotoxic types, infiltrating the liver.
  • Other immune cells like NK cells, macrophages, and B lymphocytes are also present.

Purpose of the Study:

  • To elucidate the role of T helper cell subsets and regulatory T cells in the pathogenesis of autoimmune hepatitis.
  • To understand the mechanisms of autoantigen presentation and T cell activation in AIH.
  • To explore the implications of regulatory T cell dysfunction in AIH progression.

Main Methods:

  • Histological examination of liver lesions.
  • Immunohistochemical analysis of inflammatory cell phenotypes.
  • T cell differentiation pathways (TH1/TH2) based on cytokine milieu (IL-12, IL-4).
  • Role of antigen-presenting cells and HLA molecules in T cell activation.
  • Investigation of CD4+CD25high regulatory T cells.

Main Results:

  • T helper 0 (TH0) lymphocytes differentiate into TH1 or TH2 cells, influencing liver cell vulnerability and autoantibody production.
  • TH1 cells enhance HLA class I and II expression, promoting CD8+ T cell attack and hepatocyte damage.
  • TH2 cells produce cytokines that favor B cell autoantibody production.
  • Impaired numerical and functional regulatory T cells are characteristic of AIH, leading to sustained immune responses and liver destruction.
  • AIH type 2 research, focusing on cytochrome P450IID6 (CYP2D6) autoantigen, aids in characterizing antigen-specific immune responses.

Conclusions:

  • AIH pathogenesis involves a complex interplay of effector and regulatory T cell dysfunction.
  • Dysregulation of T helper cell subsets and impaired regulatory T cell function are critical drivers of chronic liver damage in AIH.
  • Understanding these immune mechanisms, particularly in AIH type 2, offers insights for targeted therapies.