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 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.
Diabetes Mellitus: Overview and Type I Subtype01:22

Diabetes Mellitus: Overview and Type I Subtype

Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...

You might also read

Related Articles

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

Sort by
Same author

Non-HLA type 1 diabetes genes modulate disease risk together with HLA-DQ and islet autoantibodies.

Genes and immunity·2015
Same author

Attenuation of islet-specific T cell responses is associated with C-peptide improvement in autoimmune type 2 diabetes patients.

Clinical and experimental immunology·2013
Same author

Immunology in the Clinic Review Series; focus on metabolic diseases: development of islet autoimmune disease in type 2 diabetes patients: potential sequelae of chronic inflammation.

Clinical and experimental immunology·2011
Same author

Comparison of cryopreservation methods on T-cell responses to islet and control antigens from type 1 diabetic patients and controls.

Diabetes/metabolism research and reviews·2011
Same author

Current approaches to measuring human islet-antigen specific T cell function in type 1 diabetes.

Clinical and experimental immunology·2010
Same author

Changes in GAD65Ab-specific antiidiotypic antibody levels correlate with changes in C-peptide levels and progression to islet cell autoimmunity.

The Journal of clinical endocrinology and metabolism·2010

Related Experiment Video

Updated: May 8, 2026

Electrochemiluminescence Assays for Human Islet Autoantibodies
09:15

Electrochemiluminescence Assays for Human Islet Autoantibodies

Published on: March 23, 2018

Islet autoimmunity in phenotypic type 2 diabetes patients.

B Brooks-Worrell1, R Narla, J P Palmer

  • 1Department of Medicine, University of Washington, Seattle, WA, USA. bbrooks@u.washington.edu

Diabetes, Obesity & Metabolism
|September 6, 2013
PubMed
Summary

Type 2 diabetes (T2D) involves chronic inflammation and islet autoimmunity, similar to type 1 diabetes (T1D). This cell-mediated autoimmune disease contributes to beta-cell dysfunction and T2D progression.

Keywords:
T cellsautoimmune diseaseautoimmunityinflammationislet-reactive T cellstype 1 diabetestype 2 diabetes

More Related Videos

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
06:27

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Published on: May 6, 2013

Isolation of Human Islets from Partially Pancreatectomized Patients
11:10

Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Related Experiment Videos

Last Updated: May 8, 2026

Electrochemiluminescence Assays for Human Islet Autoantibodies
09:15

Electrochemiluminescence Assays for Human Islet Autoantibodies

Published on: March 23, 2018

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
06:27

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells

Published on: May 6, 2013

Isolation of Human Islets from Partially Pancreatectomized Patients
11:10

Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Area of Science:

  • Immunology
  • Endocrinology
  • Metabolic Diseases

Background:

  • Type 2 diabetes (T2D) was historically viewed as a metabolic disease of aging.
  • Emerging evidence highlights chronic systemic inflammation's role in insulin resistance and T2D development.
  • Investigations reveal islet-specific T cells and autoimmune disease in T2D patients.

Purpose of the Study:

  • To discuss the role of cell-mediated islet autoimmune disease in T2D progression.
  • To explore similarities in islet-specific T-cell reactivity between T1D and T2D.
  • To provide insights into the pathophysiology of T2D.

Main Methods:

  • Literature review and synthesis of existing research.
  • Analysis of immunological findings in T2D patients.
  • Comparative analysis of T-cell responses in T1D and T2D.

Main Results:

  • Cell-mediated islet autoimmunity is implicated in the pathogenesis of T2D.
  • Progressive loss of beta-cell function in T2D correlates with islet autoimmunity.
  • Shared T-cell reactivity patterns observed between T1D and T2D.

Conclusions:

  • Islet autoimmunity is a significant factor in T2D progression.
  • T2D shares immunological mechanisms with T1D, particularly T-cell mediated autoimmunity.
  • Understanding these shared pathways may offer new therapeutic targets for T2D.