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REVIEW article

Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1537405
This article is part of the Research Topic Community Series in Autoimmune Diabetes: Molecular Mechanisms and Neoantigens, Volume II View all 7 articles

The Role of Oxidative Post-Translational Modifications in Type 1 Diabetes Pathogenesis

Provisionally accepted
  • 1 Dasman Diabetes Institute, Kuwait City, Kuwait
  • 2 ULB Center for Diabetes Research, Université Libre de Bruxelles, Brussels, 1070, Belgium, Bruxelles, Belgium
  • 3 Department of Human Science and Promotion of Quality of Life, San Raffaele Telematic University, Rome, Lazio, Italy
  • 4 Fondazione Policlinico Universitario Campus Bio-Medico di Roma, Rome, Italy
  • 5 Campus Bio-Medico University, Rome, Lazio, Italy
  • 6 Crown Princess Victoria Children's Hospital and Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden, Linköping, Sweden
  • 7 Centre for Biochemical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, England, United Kingdom
  • 8 Dipartimento di Scienze Umane e Promozione della Qualità della Vita, Università telematica San Raffaele, Rome, Italy

The final, formatted version of the article will be published soon.

    The pathogenesis of type 1 diabetes (T1D) involves a complex interplay of genetic predisposition, immune processes, and environmental factors, leading to the selective destruction of pancreatic betacells by the immune system. Emerging evidence suggests that intrinsic beta-cell factors, including oxidative stress and post-translational modifications (PTM) of beta-cell antigens, may also contribute to their immunogenicity, shedding new light on the multifaceted pathogenesis of T1D. Over the past 30 years, neoepitopes generated by PTMs have been hypothesized to play a role in T1D pathogenesis, but their involvement has only been systematically investigated in recent years. In this review, we explored the interplay between oxidative PTMs, neoepitopes, and T1D, highlighting oxidative stress as a pivotal factor in immune system dysfunction, beta-cell vulnerability, and disease onset.

    Keywords: post-translational modifications, type 1 diabetes, Oxidative Stress, neoepitopes, Autoimmunity, Insulin, Autoantibodies, T cell

    Received: 30 Nov 2024; Accepted: 22 Jan 2025.

    Copyright: © 2025 Alhamar, Vinci, Franzese, Tramontana, Ludvigsson, Nissim and Strollo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Ahuva Nissim, Centre for Biochemical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, England, United Kingdom
    Rocky Strollo, Dipartimento di Scienze Umane e Promozione della Qualità della Vita, Università telematica San Raffaele, Rome, Italy

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.