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Related Concept Videos

Hepatitis01:25

Hepatitis

66
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.
66
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

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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...
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Autoimmune Disorders01:29

Autoimmune Disorders

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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...
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Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence...
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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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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...
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Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

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Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
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The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
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Autoimmune hepatitis.

Maria Serena Longhi, Giorgina Mieli-Vergani, Diego Vergani1

  • 1Diego Vergani, Professor of Liver Immunopathology, Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE5 9RS, UK. diego.vergani@kcl.ac.uk.

Current Pediatric Reviews
|November 19, 2014
PubMed
Summary
This summary is machine-generated.

Autoimmune hepatitis (AIH) is an aggressive liver disease. Research suggests defects in regulatory T-cells may cause AIH, offering potential new immunotherapy targets.

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Area of Science:

  • Hepatology
  • Immunology
  • Autoimmune Diseases

Background:

  • Autoimmune hepatitis (AIH) is a severe liver disease with female predominance.
  • It presents with hypertransaminasemia, elevated IgG, autoantibodies, and interface hepatitis.
  • AIH occurs in adults and children, often more aggressively in the latter.

Purpose of the Study:

  • To differentiate AIH types based on autoantibodies (ANA/SMA vs. LKM-1).
  • To compare AIH types regarding onset, presentation (fulminant hepatic failure), and IgA deficiency.
  • To explore the role of regulatory T-cells in AIH pathogenesis and potential immunotherapy.

Main Methods:

  • Classification of AIH into type 1 (ANA/SMA positive) and type 2 (LKM-1 positive).
  • Clinical comparison of AIH types based on age, presentation, and IgA levels.
  • Investigation of CD4(pos)CD25(pos) regulatory T-cell defects in AIH patients.

Main Results:

  • AIH-1 and AIH-2 differ in age of onset, frequency of fulminant hepatic failure, and IgA deficiency.
  • Standard immunosuppressive treatment (corticosteroids, azathioprine) is effective but has relapse rates (~40%) and transplant needs (~9%).
  • Evidence points to numerical and functional defects in regulatory T-cells contributing to AIH.

Conclusions:

  • AIH classification aids in understanding disease heterogeneity.
  • Immunosuppression is standard but limited by relapses and transplant requirements.
  • Defects in regulatory T-cells are implicated in AIH pathogenesis, suggesting in vitro expanded regulatory T-cells as a potential immunotherapy.