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 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 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...
Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...

You might also read

Related Articles

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

Sort by
Same author

[2025 Nobel Prize in medicine: Regulatory T cells, key players in peripheral tolerance].

La Revue du praticien·2026
Same author

Quality of antidiabetic medicines in 13 sub-Saharan African countries: a cross-sectional survey.

EClinicalMedicine·2025
Same author

IFNγ causes mitochondrial dysfunction and oxidative stress in myositis.

Nature communications·2024
Same author

First-in-human, double-blind, randomized phase 1b study of peptide immunotherapy IMCY-0098 in new-onset type 1 diabetes: an exploratory analysis of immune biomarkers.

BMC medicine·2024
Same author

Deletion of the Clock Gene <i>Bmal2</i> Leads to Alterations in Hypothalamic Clocks, Circadian Regulation of Feeding, and Energy Balance.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2024
Same author

Repositioning the Early Pathology of Type 1 Diabetes to the Extraislet Vasculature.

Journal of immunology (Baltimore, Md. : 1950)·2024

Related Experiment Video

Updated: May 16, 2026

Isolation of Human Islets from Partially Pancreatectomized Patients
11:10

Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Pancreatic islet autoimmunity.

Christian Boitard1

  • 1Inserm, U986, 75014 Paris, France. christian.boitard@htd.aphp.fr

Presse Medicale (Paris, France : 1983)
|November 28, 2012
PubMed
Summary
This summary is machine-generated.

Type 1 diabetes (T1D) involves immune cells attacking pancreatic beta cells. Understanding the specific T-cell targets is crucial for developing new diagnostic tools and immunotherapies for T1D.

More Related Videos

Electrochemiluminescence Assays for Human Islet Autoantibodies
09:15

Electrochemiluminescence Assays for Human Islet Autoantibodies

Published on: March 23, 2018

Staining Protocols for Human Pancreatic Islets
07:48

Staining Protocols for Human Pancreatic Islets

Published on: May 23, 2012

Related Experiment Videos

Last Updated: May 16, 2026

Isolation of Human Islets from Partially Pancreatectomized Patients
11:10

Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Electrochemiluminescence Assays for Human Islet Autoantibodies
09:15

Electrochemiluminescence Assays for Human Islet Autoantibodies

Published on: March 23, 2018

Staining Protocols for Human Pancreatic Islets
07:48

Staining Protocols for Human Pancreatic Islets

Published on: May 23, 2012

Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Type 1 diabetes (T1D) is an autoimmune disease affecting 10-15% of diabetes cases, with rising incidence globally.
  • Evidence points to autoimmunity, including insulitis and autoantibodies, but the precise triggers for immune tolerance failure remain unclear.
  • T1D develops multifactorially, influenced by genetics and environmental factors, with a prediabetes stage preceding clinical onset.

Purpose of the Study:

  • To elucidate the mechanisms initiating immune tolerance failure in Type 1 diabetes.
  • To identify the autoantigens targeted by T-lymphocytes in the autoimmune response against pancreatic beta cells.
  • To understand the role of T-cell responses in the pathogenesis and progression of T1D.

Main Methods:

  • Analysis of autoimmune markers in T1D, including insulitis, islet cell antibodies, and T-lymphocyte activity.
  • Investigation of the genetic associations with T1D, particularly class II major histocompatibility complex (MHC) alleles.
  • Exploration of potential environmental triggers and local islet signals in T1D development.

Main Results:

  • The immune response in T1D involves T-lymphocytes targeting pancreatic beta cells, with a significant prediabetes phase.
  • Regulatory T-cells (Treg) and invariant NKT cells play a role in suppressing autoreactive T-cells during prediabetes.
  • While infections are implicated in experimental models, definitive environmental triggers for T1D in humans are yet to be identified.

Conclusions:

  • Mapping autoantigen-derived peptides presented to CD8+ and CD4+ T-cells is essential for T1D research.
  • This peptide cartography is a critical step towards developing diagnostic T-cell assays and effective T1D immunotherapies.
  • Further research into the complex interplay of genetic, environmental, and local islet factors is needed to fully understand T1D pathogenesis.