ArticleFrontiers in immunology2025
Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed.
- Rab24 protein levels show dynamic changes in mouse tissues and human cancers.Cell and tissue research · 2026Article
- A review of autophagy in the pancreas: normal physiology and pathophysiology.Autophagy reports · 2026Review
- Determining the Half-Life of MHC Class I Molecules by Blocking Protein Synthesis Using Cycloheximide.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.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
- Glutamine metabolism and ammonia death: targeted modulation for enhanced cancer immunotherapy.Frontiers in immunology · 2025Review
- Obesity's systemic impact: exploring molecular and physiological links to diabetes, cardiovascular disease, and heart failure.Frontiers in endocrinology · 2025Review
- Cross-talk between aging resilience pathways and autoimmunity onset.Frontiers in immunology · 2025Review
- Recent advances in early diagnosis and treatment of T1D with miRNAs.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Background: Type 1 Diabetes (T1D) is caused by a combination of genetic and environmental factors that trigger autoimmune-mediated destruction of pancreatic β-cells. Defects in β-cell stress response pathways such as autophagy may play an important role in activating and/or exacerbating the immune response in disease development. Previously, we discovered that β-cell autophagy is impaired prior to the onset of T1D, implicating this pathway in T1D pathogenesis. Aims: To assess the role of autophagy in β-cell health and survival, and whether defects in autophagy render islets more immunogenic. Methods: We knocked out the critical autophagy enzyme, ATG7, in the β-cells of mice (ATG7 Results: We found that all ATG7 Conclusions: Our findings demonstrate that β-cell autophagy is critical to cell survival/function. Defective β-cell autophagy induces ER stress, alters pathways of antigen production, and enhances MHC-I/HLA-I presentation to surveilling immune cells. Overall, our results suggest that defects in autophagy make β-cells more susceptible to immune attack and destruction.
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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 Socratic graph.