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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...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

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Related Experiment Video

Updated: Jun 1, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
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IL-13Rα1 expression on β-cell-specific T cells in NOD mice.

Sarah S Rasche1, Michele Phillips, Marcia F McInerney

  • 1Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA.

Diabetes
|May 28, 2011
PubMed
Summary

Interleukin-13 (IL-13) plays a key role in regulating early-stage insulitis in diabetes-prone mice. Loss of IL-13 receptor α1 (IL-13Rα1) on T cells may indicate immune dysregulation and disease progression.

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06:27

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Observing Islet Function and Islet-Immune Cell Interactions in Live Pancreatic Tissue Slices
05:51

Observing Islet Function and Islet-Immune Cell Interactions in Live Pancreatic Tissue Slices

Published on: April 12, 2021

Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • Immunotherapy with GAD65 peptides can preserve glucose homeostasis in non-obese diabetic (NOD) mice.
  • Previous studies identified GAD65 epitopes 524-538 and 530-543, with 524-538 linked to reduced hyperglycemia.

Purpose of the Study:

  • To investigate if T cells specific for peptide p524-538 can regulate islet-reactive T cells.
  • To determine the role of IL-13 and IL-13Rα1 in the regulation of islet autoimmunity in NOD mice.

Main Methods:

  • Prediabetic NOD mice were used to study the relationship between peptide p524-538-induced IL-13 and islet autoimmunity.
  • Pancreatic lymph node (PLN) cells were analyzed for IL-13 receptor α1 (IL-13Rα1) expression on T cells at different stages of insulitis.

Main Results:

  • Peptide p524-538 induced IL-13-producing T cells that counteracted GAD65 autoimmunity and inhibited islet-reactive T cell proliferation.
  • Functional IL-13Rα1 was expressed on a subset of CD4(+) T cells, and its expression was higher in young NOD mice compared to older mice with advanced insulitis.
  • Immunization with p524-538 maintained IL-13Rα1 expression on PLN T cells.

Conclusions:

  • IL-13 is crucial for regulating autoimmunity during early insulitis stages.
  • Loss of IL-13Rα1 on islet-reactive T cells may serve as a biomarker for diminished immune regulation and progression to type 1 diabetes.