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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...
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
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...
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.
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...

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

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Changes in autoreactive T cell avidity during type 1 diabetes development.

Nathan E Standifer1, Emily A Burwell, Vivian H Gersuk

  • 1Benaroya Research Institute at Virginia Mason, Seattle, WA 98101, USA. NStand@benaroyaresearch.org

Clinical Immunology (Orlando, Fla.)
|June 2, 2009
PubMed
Summary
This summary is machine-generated.

In individuals at high risk for type 1 diabetes, T cell avidity for the GAD autoantigen increased over time. This suggests higher affinity T cell receptor (TCR) outgrowth contributes to pre-clinical type 1 diabetes development.

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Published on: July 5, 2022

Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • T cell activation relies on the avidity of the trimolecular complex (TCR, antigen, MHC).
  • Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic beta cells.
  • Glutamic acid decarboxylase (GAD) is a key autoantigen in T1D pathogenesis.

Purpose of the Study:

  • To investigate changes in CD4+ T cell avidity for GAD autoantigen in individuals at high risk for T1D.
  • To determine if T cell avidity maturation occurs during the pre-clinical stage of T1D.

Main Methods:

  • Comparison of CD4+ T cell avidity for GAD 555-567 using serial samples from autoantibody-positive, at-risk subjects.
  • Analysis of T cell receptor (TCR) BV gene expression and tetramer-binding levels.
  • Comparative analysis in autoantibody-negative relatives and T1D patients.

Main Results:

  • Significant increases in CD4+ T cell avidity for GAD 555-567 were observed in three at-risk subjects over time.
  • This avidity shift correlated with the expansion of T cells expressing specific TCR BV genes (9, 15, 17, 20) with higher GAD tetramer-binding.
  • No similar avidity changes were detected in autoantibody-negative relatives or T1D patients.

Conclusions:

  • The data suggest antigen-specific T cell avidity maturation occurs during the pre-clinical stage of T1D.
  • Outgrowth of T cells expressing higher affinity TCRs may play a role in T1D pathogenesis.
  • T cell avidity serves as a potential biomarker for T1D progression.