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Area of Science:

  • Endocrinology
  • Immunology
  • Pathology

Background:

  • Type 1 diabetes (T1D) involves immune-mediated destruction of insulin-producing beta cells.
  • The precise timing and nature of beta cell loss, especially in early T1D, are not fully understood.
  • Identifying early changes in islet composition is key to developing strategies to halt T1D progression.

Purpose of the Study:

  • To investigate the changes in pancreatic islet size and cellular composition during the development of T1D.
  • To determine which specific islet components are lost first in the progression of T1D.
  • To analyze the impact of autoantibody positivity and disease duration on islet structure.

Main Methods:

  • Developed a whole-slide image analysis pipeline for quantitative assessment of pancreatic tissue.
  • Analyzed 145 human pancreata from donors without diabetes, with autoantibody positivity, and with varying durations of T1D.
  • Quantified endocrine area, islet frequency, interislet distance, and endocrine object size distribution.

Main Results:

  • T1D pancreata showed decreased islet frequency and increased interislet distance compared to controls.
  • Significant loss of insulin-positive (INS+) single cells, cell clusters, and small-to-medium sized islets was observed at T1D onset.
  • Large INS+ islets (>200 μm) were preserved, and changes in INS+ islet fraction were noted even in multiple autoantibody-positive donors.
  • These findings suggest a preferential loss of smaller INS+ endocrine objects early in T1D.

Conclusions:

  • The early stages of T1D are characterized by the preferential loss of smaller insulin-positive endocrine cells and cell clusters.
  • Preservation of larger islets suggests a specific vulnerability of smaller structures to autoimmune destruction in T1D.
  • These insights are critical for understanding T1D pathogenesis and for designing targeted therapeutic interventions.