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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...
Diabetes: Symptoms, Diagnosis, and Complications01:15

Diabetes: Symptoms, Diagnosis, and Complications

For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is based on...
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 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...
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.

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Related Experiment Video

Updated: Jul 18, 2026

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

[Decrease of FOXP3 mRNA in CD4+ T cells in latent autoimmune diabetes in adult].

Zhi-fang Yang1, Zhi-guang Zhou, Wei-li Tang

  • 1Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Diabetes Center of Central South University, Changsha 410011, China.

Zhonghua Yi Xue Za Zhi
|January 3, 2007
PubMed
Summary

In latent autoimmune diabetes in adults (LADA), CD4(+)CD25(+) T cells are increased, but FOXP3 mRNA expression is decreased, suggesting impaired regulatory T cell function. This finding is crucial for understanding LADA pathogenesis.

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In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
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In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction

Published on: January 22, 2020

Area of Science:

  • Immunology
  • Endocrinology
  • Diabetes Research

Context:

  • Latent autoimmune diabetes in adults (LADA) is an autoimmune form of diabetes with features of both type 1 and type 2 diabetes.
  • Understanding the immunological underpinnings of LADA is critical for developing targeted therapies.
  • Regulatory T cells (Tregs) play a key role in maintaining immune tolerance and preventing autoimmune diseases.

Purpose:

  • To investigate the percentage of peripheral blood CD4(+)CD25(+) T cells and the expression of FOXP3 mRNA in patients with LADA.
  • To compare these immune cell populations and gene expression levels with those in patients with type 2 diabetes and healthy controls.

Summary:

  • Patients with LADA exhibited a significantly higher percentage of CD4(+)CD25(+) T cells and a lower CD4(+)/CD8(+) T cell ratio compared to healthy controls.
  • Despite increased CD4(+)CD25(+) T cells, FOXP3 mRNA expression in CD4(+) T cells was significantly lower in LADA patients.
  • The percentage of CD4(+)CD25(+) T cells positively correlated with glutamic acid decarboxylase antibody (GADA) titers in LADA patients.

Impact:

  • The findings suggest a potential defect in the suppressor function of regulatory T cells in LADA.
  • This research contributes to a deeper understanding of the immunopathogenesis of LADA.
  • Identifying immune dysregulation in LADA may pave the way for novel therapeutic strategies targeting T cell function.