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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...
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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...
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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...

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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
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Dipeptidyl peptidase in autoimmune pathophysiology.

Kei Ohnuma1, Osamu Hosono, Nam H Dang

  • 1Division of Rheumatology and Allergy, Research Hospital, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo, Japan.

Advances in Clinical Chemistry
|March 17, 2011
PubMed
Summary

CD26, a protein with dipeptidyl peptidase IV (DPPIV) activity, plays a crucial role in immune regulation and T cell activation. Targeting CD26 offers potential therapeutic strategies for immune disorders.

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • CD26 is a surface glycoprotein with dipeptidyl peptidase IV (DPPIV) enzymatic activity.
  • It is expressed on various immune cells and involved in critical immunological functions.
  • CD26's role in immune regulation, T cell activation, and autoimmune pathogenesis is increasingly recognized.

Purpose of the Study:

  • To review the biological functions of CD26, focusing on its peptidase activity.
  • To elucidate CD26's association with signaling pathways in T cell activation and antigen-presenting cell interactions.
  • To assess CD26 as a potential therapeutic target for immune disorders.

Main Methods:

  • Utilizing anti-CD26 antibodies and chemical inhibitors to modulate CD26/DPPIV activity.
  • Employing siRNAs for CD26 gene silencing and overexpressing CD26 transfectants.
  • Investigating CD26 interactions using soluble CD26 molecules and proteomic approaches.

Main Results:

  • CD26/DPPIV activity is integral to its function in immune regulation.
  • CD26 physically and functionally associates with key molecules in immune signaling.
  • Experimental modulation of CD26 impacts T cell responses and cellular functions.

Conclusions:

  • CD26 is intricately linked to T cell activation and immune cell interactions.
  • Its involvement in autoimmune pathogenesis highlights its clinical relevance.
  • Emerging data support CD26 as a viable therapeutic target for specific immune conditions.