ArticleDiabetologia2011
Immunohistochemical analysis of the relationship between islet cell proliferation and the production of the enteroviral capsid protein, VP1, in the islets of patients with recent-onset type 1 diabetes.
Article in Diabetologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 52 citations in OpenAlex.
- Immunological and virological triggers of type 1 diabetes: insights and implications.Frontiers in immunology · 2023Review
- Review
- Increased Expression of Viral Sensor MDA5 in Pancreatic Islets and in Hormone-Negative Endocrine Cells in Recent Onset Type 1 Diabetic Donors.Frontiers in immunology · 2022Article
- Persistence of Coxsackievirus B4 in Pancreatic β Cells Disturbs Insulin Maturation, Pattern of Cellular Proteins, and DNA Methylation.Microorganisms · 2021Article
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- Long Non-Coding RNAs as Key Modulators of Pancreatic β-Cell Mass and Function.Frontiers in endocrinology · 2020Review
- Pancreatic beta cells persistently infected with coxsackievirus B4 are targets of NK cell-mediated cytolytic activity.Cellular and molecular life sciences : CMLS · 2020Article
- How, When, and Where Do Human β-Cells Regenerate?Current diabetes reports · 2019Review
- Enteroviral infections in the pathogenesis of type 1 diabetes: new insights for therapeutic intervention.Current opinion in pharmacology · 2018Review
- Persistence of Coxsackievirus B4 in pancreatic ductal-like cells results in cellular and viral changes.Virulence · 2017Article
- Type 1 Diabetes and Type 1 Interferonopathies: Localization of a Type 1 Common Thread of Virus Infection in the Pancreas.EBioMedicine · 2017Review
- [Insulitis in type 1 diabetes].Der Pathologe · 2016Review
- Viral infections in type 1 diabetes mellitus--why the β cells?Nature reviews. Endocrinology · 2016Review
- Mechanisms of Beta Cell Dysfunction Associated With Viral Infection.Current diabetes reports · 2015Review
- Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.Virology · 2015Review
- The subcellular distribution of cyclin-D1 and cyclin-D3 within human islet cells varies according to the status of the pancreas donor.Diabetologia · 2015Article
- Heterogeneity and Lobularity of Pancreatic Pathology in Type 1 Diabetes during the Prediabetic Phase.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2015Article
- Viral infection of engrafted human islets leads to diabetes.Diabetes · 2015Article
- Enterovirus infection is associated with an increased risk of childhood type 1 diabetes in Taiwan: a nationwide population-based cohort study.Diabetologia · 2015Article
- Potential viral pathogenic mechanism in human type 1 diabetes.Diabetologia · 2014Review
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe enteroviral capsid protein, VP1, was recently shown to be present in some beta cells in more than 60% of patients with recent-onset type 1 diabetes but in very few age-matched controls. The rate of proliferation of islet cells was also markedly increased in the type 1 diabetic patients. As it has been suggested that enteroviruses replicate most efficiently in proliferating cells, we have investigated whether VP1 is preferentially present in proliferating beta cells in type 1 diabetes.
methodsCombined immunoperoxidase and immunofluorescence staining was used to record the presence of enteroviral VP1, insulin and Ki67 in the islets of recent-onset type 1 diabetic patients.
resultsFrom a total of 1,175 islets, 359 (30.5%) contained insulin. VP1-producing endocrine cells were found in 72 islets (6.1% of total), all of which retained insulin. Ki67(+) endocrine cells were present in 52 (4.4%) islets, with 44 (84.6%) of these being insulin-positive. Overall, 28 of 1,175 (2.4%) islets contained both Ki67(+) cells and VP1(+) cells. Dual positivity of these markers accounted for 38.9% of the total VP1(+) islets and 53.8% of the total Ki67(+) islets. No individual islet cells were dual-positive for Ki67 and VP1. CONCLUSIONS/
interpretationKi67(+) cells were frequently observed in islets that also contained VP1(+) cells, suggesting that the factors facilitating viral replication may also drive islet cell proliferation. However, in an individual cell, VP1 production does not require concurrent beta cell proliferation.
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