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Related Experiment Videos

Immune regulation in type 1 diabetes

A Shimada1, B Charlton, P Rohane

  • 1Department of Medicine, Stanford University School of Medicine, CA 94305, USA.

Journal of Autoimmunity
|April 1, 1996
PubMed
Summary

Immune regulatory cells in non-obese diabetic (NOD) mice, specifically memory CD4+ cells, delay diabetes onset. Their function shifts from protective to pathogenic, influencing disease progression in this insulin-dependent diabetes mellitus model.

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Area of Science:

  • Immunology
  • Endocrinology
  • Diabetes Research

Background:

  • The non-obese diabetic (NOD) mouse model mimics human insulin-dependent diabetes mellitus (IDDM).
  • A gap exists between insulitis onset and diabetes in NOD mice, suggesting immune regulation.
  • Immune regulatory cells potentially delay pancreatic beta cell destruction.

Purpose of the Study:

  • To investigate the role of immune regulatory cells in NOD mice.
  • To identify the characteristics and function of these regulatory cells.
  • To understand how these cells influence the progression of autoimmune diabetes.

Main Methods:

  • Utilized a transfer system with NOD-scid/scid mice receiving donor NOD cells.
  • Analyzed peripheral immune cells, focusing on CD4+ CD45RBlow (memory) T cells.

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  • Assessed cytokine profiles (Th1/Th2) following in vitro activation.

    • Main Results:

    • Immune regulatory cells were found in the periphery, not islets, of NOD mice.
    • These cells are identified as memory CD4+ T cells with an initial Th2/Th0 cytokine profile.
    • A functional shift from protective to pathogenic occurred, with a cytokine profile change to Th1 preceding hyperglycemia.

    Conclusions:

    • CD4+ CD45RBlow immune regulatory cells control the progression of NOD disease.
    • The shift in their function and cytokine profile is linked to the transition from insulitis to overt diabetes.
    • Understanding these regulatory mechanisms is crucial for IDDM research.