ArticleCell metabolism2017
β Cells that Resist Immunological Attack Develop during Progression of Autoimmune Diabetes in NOD Mice.
Article in Cell metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 1 of them a synthesis that pooled it.
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Who cites it
141 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Footprints of the Immune Assault on Pancreatic Beta Cells in Type 1 Diabetes.Frontiers in endocrinology · 2020Pooled it
- Interleukin-1 mediates innate immune signaling and antiviral defense in islets.Life science alliance · 2026Article
- Dual Modulation of Prostaglandin E2 Receptors EP3 and EP4 Protects β-Cell Mass in a Model of Aggressive Autoimmune Inflammation.Diabetes · 2026Article
- GLP1-E2 therapy delays autoimmune diabetes in late-stage prediabetic NOD mice and potentiates low-dose anti-CD3 therapy for enhanced disease protection.Diabetologia · 2026Article
- Immune Checkpoint Inhibitor-Induced Diabetes Presenting As Diabetic Ketoacidosis: A Case Report.Cureus · 2026Article
- Imaging mass cytometry reveals functional and immunological changes during type 1 diabetes progression in human pancreata.Nature metabolism · 2026Article
- A surviving beta cell subpopulation enriched in patients with T1D.bioRxiv : the preprint server for biology · 2026Article
- A mitochondrial ROS-dependent antiviral response promotes β cell resilience and is diminished in donors with type 1 diabetes.Science translational medicine · 2026Article
- Beyond bystanders: How β cell stress shapes the autoimmune response in T1D.Science translational medicine · 2026Review
- Tet2 modulates ER stress responses related to β-cell death and autoimmunity in diabetes.iScience · 2026Article
- Calorie Restriction Upregulates Islet PD-L1 Signaling and Decreases the Risk of Autoimmune Diabetes Onset in NOD Mice.bioRxiv : the preprint server for biology · 2026Article
- Anti-CD3 mAb treatment reshapes infiltrating T and β cells in the islets in autoimmune diabetes.JCI insight · 2026Article
- Islet-intrinsic sex differences in inflammatory signaling contribute to autoimmune diabetes susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Spatially bound functional heterogeneity drives modular organization in β-cell networks.Biophysical journal · 2025Article
- Checkpoint Inhibitor-Induced Autoimmune Diabetes: An Autoinflammatory Disease.Cold Spring Harbor perspectives in medicine · 2025Review
- IFN-α Induces Heterogenous ROS Production in Human β-Cells.bioRxiv : the preprint server for biology · 2025Article
- Beta cell extracellular vesicle PD-L1 as a novel regulator of CD8Diabetologia · 2025Article
- Detection of Insulin in Insulin-Deficient Islets of Patients with Type 1 Diabetes.Life (Basel, Switzerland) · 2025Article
- Immune checkpoint inhibitor-associated diabetes mellitus: mechanisms, clinical manifestations, and management strategies.Frontiers in endocrinology · 2025Review
- Sensing danger in the islet: the roles of pattern recognition receptors in β cells and type 1 diabetes.Frontiers in immunology · 2025Review
81 more citing papers are in PubMed but not listed here.
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6 authors.
Funding
Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disease that involves immune-mediated destruction of β cells. How β cells respond to immune attack is unknown. We identified a population of β cells during the progression of T1D in non-obese diabetic (NOD) mice that survives immune attack. This population develops from normal β cells confronted with islet infiltrates. Pathways involving cell movement, growth and proliferation, immune responses, and cell death and survival are activated in these cells. There is reduced expression of β cell identity genes and diabetes antigens and increased immune inhibitory markers and stemness genes. This new subpopulation is resistant to killing when diabetes is precipitated with cyclophosphamide. Human β cells show similar changes when cultured with immune cells. These changes may account for the chronicity of the disease and the long-term survival of β cells in some patients.
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