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The role of oxidative post-translational modifications in type 1 diabetes pathogenesis

Ghadeer Alhamar1, Chiara Vinci2, Valentina Franzese3,4,5

  • 1Department of Immunology and Microbiology, Dasman Diabetes Institute, Dasman, Kuwait.

Frontiers in Immunology
|March 3, 2025
PubMed

Insights

Oxidative stress and post-translational modifications (PTM) create neoepitopes, increasing beta-cell vulnerability and driving type 1 diabetes (T1D) pathogenesis. This review explores their pivotal role in immune dysfunction and disease onset.

Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • Type 1 diabetes (T1D) pathogenesis involves genetic, immune, and environmental factors.
  • Pancreatic beta-cell destruction is a hallmark of T1D.
  • Emerging evidence points to intrinsic beta-cell factors in T1D development.

Purpose of the Study:

  • To review the interplay between oxidative post-translational modifications (PTMs), neoepitopes, and T1D.
  • To highlight oxidative stress as a key factor in T1D pathogenesis.

Main Methods:

  • Literature review focusing on oxidative PTMs and neoepitopes in T1D.
  • Analysis of recent investigations into PTM-generated neoepitopes.

Main Results:

  • Oxidative stress contributes to beta-cell vulnerability and immune dysfunction.
  • PTMs generate neoepitopes that may enhance beta-cell immunogenicity.
  • Neoepitopes from PTMs are increasingly recognized in T1D pathogenesis.

Conclusions:

  • Oxidative PTMs and resulting neoepitopes are significant contributors to T1D pathogenesis.
  • Oxidative stress plays a pivotal role in immune system dysfunction and beta-cell targeting in T1D.
  • Further research into these mechanisms can illuminate T1D onset and inform therapeutic strategies.
Keywords:
autoantibodiesautoimmunityinsulinneoepitopesoxidative stresspost-translational modificationst celltype 1 diabetes

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