ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2015
Heterogeneity and Lobularity of Pancreatic Pathology in Type 1 Diabetes during the Prediabetic Phase.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed.
- Review
- Single-Islet Proteomics Maps Pseudo-Temporal Islet Immune Responses and Dysfunction in Stage 1 Type 1 Diabetes.bioRxiv : the preprint server for biology · 2025Article
- Whole tissue spatial cellular analysis reveals increased macrophage infiltration in pancreata of autoantibody positive donors and patients with type 1 diabetes.bioRxiv : the preprint server for biology · 2025Article
- Enterovirus VP1 protein and HLA class I hyperexpression in pancreatic islet cells of organ donors with type 1 diabetes.Diabetologia · 2025Article
- Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.Frontiers in immunology · 2025Article
- Macrophages: friend or foe in diabetes pathogenesis and therapy.Frontiers in immunology · 2025Review
- Review
- Type 1 diabetes: immune pathology and novel therapeutic approaches.Diabetology international · 2024Review
- The immunomodulator effect ofFood science & nutrition · 2024Article
- Teplizumab's immunomodulatory effects on pancreatic β-cell function in type 1 diabetes mellitus.Clinical diabetes and endocrinology · 2024Review
- Impaired islet function and normal exocrine enzyme secretion occur with low inter-regional variation in type 1 diabetes.Cell reports · 2024Article
- Insulitis in human type 1 diabetes: lessons from an enigmatic lesion.European journal of endocrinology · 2024Article
- Disrupted RNA editing in beta cells mimics early-stage type 1 diabetes.Cell metabolism · 2024Article
- Network approach reveals preferential T-cell and macrophage association with α-linked β-cells in early stage of insulitis in NOD mice.Frontiers in network physiology · 2024Article
- Cutting edge of immune response and immunosuppressants in allogeneic and xenogeneic islet transplantation.Frontiers in immunology · 2024Review
- The beta cell-immune cell interface in type 1 diabetes (T1D).Molecular metabolism · 2023Review
- Particle-Based therapies for antigen specific treatment of type 1 diabetes.International journal of pharmaceutics · 2023Review
- The role of the interferon/JAK-STAT axis in driving islet HLA-I hyperexpression in type 1 diabetes.Frontiers in endocrinology · 2023Review
- Review
- Evidence of islet CADM1-mediated immune cell interactions during human type 1 diabetes.JCI insight · 2022Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Type 1 diabetes (T1D) is an autoimmune disease in which insulin-producing beta cells are destroyed in the islets of Langerhans. One of its main pathological manifestations is the hyper-expression of Major Histocompatibility Complex I (MHC-I) by beta cells, which was first described over 3 decades ago yet its cause remains unknown. It might not only be a sign of beta cell dysfunction but could also render the cells susceptible to autoimmune destruction; for example, by islet-infiltrating CD8 T cells. In this report, we studied pancreas tissue from a 22-year-old non-diabetic male cadaveric organ donor who had been at high risk of developing T1D, in which autoantibodies against GAD and IA-2 were detected. Pancreas sections were analyzed for signs of inflammation. Multiple insulin-containing islets were identified, which hyper-expressed MHC-I. However, islet density and MHC-I expression exhibited a highly lobular and heterogeneous pattern even within the same section. In addition, many islets with high expression of MHC-I presented higher levels of CD8 T cell infiltration than normal islets. These results demonstrate the heterogeneity of human pathology that occurs early during the pre-diabetic, autoantibody positive phase, and should contribute to the understanding of human T1D.
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