ReviewFrontiers in immunology2026
Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Drug-tolerant persister cells use conserved adaptive transcriptional programs.Translational cancer research · 2026Article
- Structural Remodeling of TCR-HLA-DQ8 Recognition by a β-Cell Stress-Associated C19S Insulin Neoepitope in Type 1 Diabetes.International journal of molecular sciences · 2026Article
- Nitration in cancer signaling.Redox biology · 2026Review
- Oxidative-Stress-Associated Molecular Signatures in Immune-Mediated Diseases: A Systematic Review Integrating Machine Learning and Systems Biology Approaches.Antioxidants (Basel, Switzerland) · 2026Review
- A multi-level machine learning pipeline for prediction and prioritization of hybrid insulin peptides in type 1 diabetes.Frontiers in immunology · 2026Article
- Nardilysin: classical functions and new horizons in autoimmunity.Frontiers in immunology · 2026Review
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is an autoimmune disorder driven by progressive destruction of pancreatic β-cells under conditions of metabolic and oxidative stress. This article examines the intersection of immunometabolism and antigen presentation as a central mechanism in T1D pathogenesis. In β-cells, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and redox imbalance remodel the immunopeptidome, promoting neoepitope formation and upregulation of major histocompatibility complex class I (MHC-I) molecules. Concurrently, antigen-presenting cells (APCs) exposed to hypoxia, cytokines, and nutrient deprivation undergo metabolic reprogramming that enhances glycolysis, reactive oxygen species (ROS) production, and pro-inflammatory antigen processing. These parallel responses establish a self-sustaining β-cell-APC loop in which metabolic distress in one cell type amplifies dysfunction in the other. By integrating evidence from redox signaling, immunopeptidomics, and metabolic regulation, this perspective defines a unified framework wherein metabolism acts as both initiator and amplifier of autoimmunity. Targeting the immunometabolic interface between β-cells and APCs may restore immune tolerance and prevent disease progression by re-establishing cellular homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.