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Tumor necrosis factor-related apoptosis-inducing ligand and CD56 expression in patients with type 1 diabetes mellitus

Sze-shuen C Cheung1, Daniel L Metzger, Xiaojie Wang

  • 1Department of Pediatrics, Faculty of Medicine, The University of British Columbia, Vancouver, British Columbia, Canada.

Pancreas
|February 17, 2005
PubMed
Abstract

Insights

Immune cells expressing CD56 and the cytokine TRAIL are present during pancreatic beta-cell destruction in type 1 diabetes (T1D). These markers appear on T-cells activated by beta-cell antigens in new-onset T1D.

Area of Science:

  • Immunology
  • Endocrinology
  • Pathology

Background:

  • Previous research indicated that CD56+ T-cells and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) contribute to human pancreatic beta-cell destruction in vitro.
  • The role of these specific immune components during the early stages of type 1 diabetes (T1D) in vivo remained to be elucidated.

Purpose of the Study:

  • To investigate the presence and significance of CD56 and TRAIL during islet cell destruction at the clinical onset of type 1 diabetes mellitus (T1D).
  • To analyze T-cell marker and cytokine expression in pancreatic islets of children with acute-onset T1D and in T-cell lines from new-onset T1D patients.

Main Methods:

  • Immunohistochemistry was employed to examine TRAIL, CD56, and other T-cell markers on pancreatic islet sections from two children with acute-onset T1D.
  • Flow cytometry was utilized to analyze TRAIL and CD56 expression in antigen-activated T-cell lines derived from 29 children with new-onset T1D.

Main Results:

  • TRAIL-positive (TRAIL+), CD56-positive (CD56+), CD45RO+, and CD3+ immune cells were identified within the islets of patients with acute-onset T1D.
  • These specific immune cells were notably absent in normal pancreatic islets.
  • T-cell lines from new-onset T1D patients demonstrated TRAIL and CD56 expression upon stimulation with key beta-cell antigens: GAD, IA-2, and the insulin beta chain.

Conclusions:

  • The findings confirm that TRAIL and CD56 expression are integral components of the T-cell-mediated immune response involved in pancreatic beta-cell destruction.
  • This suggests a potential role for these markers in the pathogenesis of type 1 diabetes.

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