ArticleDiabetes2019
The Immunoreactive Platform of the Pancreatic Islets Influences the Development of Autoreactivity.
Article in Diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Discovery of Post-Translationally Modified Epitopes in Autoimmunity: Someone Has to Fish so Everyone Can Eat.Immunological reviews · 2026Review
- Type 1 Diabetes: A Guide to Autoimmune Mechanisms for Clinicians.Diabetes, obesity & metabolism · 2025Review
- Two DRB3 residues predictively associate with the progression to type 1 diabetes among DR3 carriers.JCI insight · 2025Article
- Interactions between islet-resident macrophages and β cells in diabetes.Frontiers in immunology · 2025Review
- Macrophages: friend or foe in diabetes pathogenesis and therapy.Frontiers in immunology · 2025Review
- Oral Insulin Delay of Stage 3 Type 1 Diabetes Revisited in HLA DR4-DQ8 Participants in the TrialNet Oral Insulin Prevention Trial (TN07).Diabetes care · 2024Article
- CXCL16-dependent scavenging of oxidized lipids by islet macrophages promotes differentiation of pathogenic CD8Immunity · 2024Article
- Single-cell multi-omics analysis of human pancreatic islets reveals novel cellular states in type 1 diabetes.Nature metabolism · 2022Article
- 12-Lipoxygenase governs the innate immune pathogenesis of islet inflammation and autoimmune diabetes.JCI insight · 2021Article
- Neoepitopes in Type 1 Diabetes: Etiological Insights, Biomarkers and Therapeutic Targets.Frontiers in immunology · 2021Article
- Review
- Presumption of innocence for beta cells: why are they vulnerable autoimmune targets in type 1 diabetes?Diabetologia · 2020Review
- Localized Immunosuppression With Tannic Acid Encapsulation Delays Islet Allograft and Autoimmune-Mediated Rejection.Diabetes · 2020Article
- Article
- Characterization of Proinsulin T Cell Epitopes Restricted by Type 1 Diabetes-Associated HLA Class II Molecules.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Tissue homeostasis is maintained through a finely tuned balance between the immune system and the organ-resident cells. Disruption of this process not only results in organ dysfunction but also may trigger detrimental autoimmune responses. The islet of Langerhans consists of the insulin-producing β-cells essential for proper control of body metabolism, but less appreciated is that these cells naturally interact with the immune system, forming a platform by which the β-cell products are sensed, processed, and responded to by the local immune cells, particularly the islet-resident macrophages. Although its physiological outcomes are not completely understood, this immunoreactive platform is crucial for precipitating islet autoreactivity in individuals carrying genetic risks, leading to the development of type 1 diabetes. In this Perspective, we summarize recent studies that examine the cross talk between the β-cells and various immune components, with a primary focus on discussing how antigenic information generated during normal β-cell catabolism can be delivered to the resident macrophage and further recognized by the adaptive CD4 T-cell system, a critical step to initiate autoimmune diabetes. The core nature of the islet immune platform can be extrapolated to other endocrine tissues and may represent a common mechanism underlying the development of autoimmune syndromes influencing multiple endocrine organs.
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Registered trials
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