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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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...
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...

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Related Experiment Video

Updated: May 16, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
10:27

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis

Published on: December 15, 2011

Polyglandular autoimmune syndrome type II.

George J Kahaly1

  • 1Gutenberg University Medical Center, Department of Medicine I, 55101 Mainz, Germany. gkahaly@uni-mainz.de

Presse Medicale (Paris, France : 1983)
|November 20, 2012
PubMed
Summary

Polyglandular autoimmune syndromes (PAS) involve multiple autoimmune disorders. Genetic susceptibility, particularly involving human leucocyte antigen (HLA) genes, is key, but environmental factors also play a role in developing these conditions.

Area of Science:

  • Immunology
  • Genetics
  • Endocrinology

Background:

  • Polyglandular autoimmune syndromes (PAS) are a group of autoimmune disorders affecting multiple endocrine glands.
  • PAS is classified into juvenile (PAS I) and adult (PAS II) types.
  • Key features include lymphocyte infiltration, organ-specific autoantibodies, immune defects, and associations with human leucocyte antigen (HLA) genes.

Purpose of the Study:

  • To explore the genetic and immunological underpinnings of polyglandular autoimmune syndromes.
  • To understand the diagnostic and prognostic value of autoantibodies in PAS.
  • To identify genetic susceptibility factors for PAS I and PAS II.

Main Methods:

  • Review of existing literature on the pathophysiology of PAS.
  • Analysis of genetic associations, including HLA, CTLA-4, and PTPN22 genes.

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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
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Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
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  • Discussion of autoantibody detection for diagnosis and risk assessment.
  • Main Results:

    • Autoantibodies serve as diagnostic markers and can identify at-risk individuals.
    • Genetic susceptibility, primarily linked to HLA genes, is necessary but not sufficient for disease development.
    • Specific genes like HLA, CTLA-4, and PTPN22 are associated with increased risk for PAS II.

    Conclusions:

    • Understanding genetic defects and environmental triggers is crucial for developing targeted therapies for organ-specific autoimmunity.
    • Immunotherapeutic approaches successful in one autoimmune disorder may benefit related conditions.
    • Further research into the interplay of genetics and environment is needed for effective treatment strategies.