ReviewThe review of diabetic studies : RDS2012
Pathogenic mechanisms in type 1 diabetes: the islet is both target and driver of disease.
Review in The review of diabetic studies : RDS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Association between telomere length and diabetes mellitus: A meta-analysis.The Journal of international medical research · 2016Pooled it
- In Vitro Evaluation of Necrostatin-1 Microparticles for Limiting Stress-induced Cell Death and Preserving Islet Function.Transplantation direct · 2026Article
- RIP kinase inhibition with Necrostatin-1 improves human marginal mass islet graft survival and function for the management of type 1 diabetes.Cell death & disease · 2026Article
- Application potential of induced pluripotent stem cells in the research and treatment of autoimmune diseases (Review).Molecular medicine reports · 2025Review
- Vitamin D Supplementation as a Therapeutic Strategy in Autoimmune Diabetes: Insights and Implications for LADA Management.Nutrients · 2024Review
- Particle-Based therapies for antigen specific treatment of type 1 diabetes.International journal of pharmaceutics · 2023Review
- Pathological mechanisms of type 1 diabetes in children: investigation of the exosomal protein expression profile.Frontiers in endocrinology · 2023Article
- Article
- Endosomal Sequestration of TLR4 Antibody Induces Myeloid-Derived Suppressor Cells and Reverses Acute Type 1 Diabetes.Diabetes · 2022Article
- The future treatment for type 1 diabetes: Pig islet- or stem cell-derived β cells?Frontiers in endocrinology · 2022Review
- Hybrid computational modeling demonstrates the utility of simulating complex cellular networks in type 1 diabetes.PLoS computational biology · 2021Article
- Thymic atrophy creates holes in Treg-mediated immuno-regulation via impairment of an antigen-specific clone.Immunology · 2021Article
- Modeling Type 1 Diabetes Using Pluripotent Stem Cell Technology.Frontiers in endocrinology · 2021Review
- Beta Cell Therapies for Preventing Type 1 Diabetes: From Bench to Bedside.Biomolecules · 2020Review
- IL-17F induces inflammation, dysfunction and cell death in mouse islets.Scientific reports · 2020Article
- Antidiabetic Potential ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Review
- IL-21 regulates SOCS1 expression in autoreactive CD8Scientific reports · 2019Article
- LPS enhances CTB-INSULIN induction of IDO1 and IL-10 synthesis in human dendritic cells.Cellular immunology · 2019Article
- eIF5A inhibition influences T cell dynamics in the pancreatic microenvironment of the humanized mouse model of Type 1 Diabetes.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent advances in our understanding of the pathogenesis of type 1 diabetes have occurred in all steps of the disease. This review outlines the pathogenic mechanisms utilized by the immune system to mediate destruction of the pancreatic beta-cells. The autoimmune response against beta-cells appears to begin in the pancreatic lymph node where T cells, which have escaped negative selection in the thymus, first meet beta-cell antigens presented by dendritic cells. Proinsulin is an important antigen in early diabetes. T cells migrate to the islets via the circulation and establish insulitis initially around the islets. T cells within insulitis are specific for islet antigens rather than bystanders. Pathogenic CD4⁺ T cells may recognize peptides from proinsulin which are produced locally within the islet. CD8⁺ T cells differentiate into effector T cells in islets and then kill beta-cells, primarily via the perforin-granzyme pathway. Cytokines do not appear to be important cytotoxic molecules in vivo. Maturation of the immune response within the islet is now understood to contribute to diabetes, and highlights the islet as both driver and target of the disease. The majority of our knowledge of these pathogenic processes is derived from the NOD mouse model, although some processes are mirrored in the human disease. However, more work is required to translate the data from the NOD mouse to our understanding of human diabetes pathogenesis. New technology, especially MHC tetramers and modern imaging, will enhance our understanding of the pathogenic mechanisms.
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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.