ArticleDiabetes2010
Phagocytosis of enterovirus-infected pancreatic beta-cells triggers innate immune responses in human dendritic cells.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- ProtectiveiScience · 2026Article
- Protocol to stress human primary pancreatic islets with diabetogenic factors for subsequent single-cell RNA sequencing.STAR protocols · 2026Article
- The gut virome and regulatory T cell axis in health and systemic disease.Microbiome research reports · 2026Review
- Coxsackievirus B infection invokes unique cell-type-specific responses in primary human pancreatic islets.Cell reports · 2025Article
- Systematic review of type 1 diabetes biomarkers reveals regulation in circulating proteins related to complement, lipid metabolism, and immune response.Clinical proteomics · 2023Review
- Pterostilbene, an active constituent of blueberries, enhances innate immune activation and restricts enterovirus D68 infection.Frontiers in immunology · 2023Article
- Identifying target ion channel-related genes to construct a diagnosis model for insulinoma.Frontiers in genetics · 2023Article
- Article
- Enteroviruses and Type 1 Diabetes: Multiple Mechanisms and Factors?Annual review of medicine · 2022Review
- IRE1α Implications in Endoplasmic Reticulum Stress-Mediated Development and Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2018Review
- Environmental Factors Contribute to β Cell Endoplasmic Reticulum Stress and Neo-Antigen Formation in Type 1 Diabetes.Frontiers in endocrinology · 2017Article
- Distinct activation of primary human BDCA1(+) dendritic cells upon interaction with stressed or infected β cells.Clinical and experimental immunology · 2016Article
- Antiviral Activity of Oroxylin A against Coxsackievirus B3 Alleviates Virus-Induced Acute Pancreatic Damage in Mice.PloS one · 2016Article
- β cell ER stress and the implications for immunogenicity in type 1 diabetes.Frontiers in cell and developmental biology · 2015Review
- Enterovirus-infected β-cells induce distinct response patterns in BDCA1+ and BDCA3+ human dendritic cells.PloS one · 2015Article
- Type I diabetes mellitus: genetic factors and presumptive enteroviral etiology or protection.Journal of pathogens · 2014Review
- Type 1 diabetes: translating mechanistic observations into effective clinical outcomes.Nature reviews. Immunology · 2013Review
- Article
- Differential susceptibility and response of primary human myeloid BDCA1(+) dendritic cells to infection with different Enteroviruses.PloS one · 2013Article
- Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production.Virology journal · 2012Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveType 1 diabetes is a chronic endocrine disorder in which enteroviruses, such as coxsackie B viruses and echoviruses, are possible environmental factors that can trigger or accelerate disease. The development or acceleration of type 1 diabetes depends on the balance between autoreactive effector T-cells and regulatory T-cells. This balance is particularly influenced by dendritic cells (DCs). The goal of this study was to investigate the interaction between enterovirus-infected human pancreatic islets and human DCs. RESEARCH DESIGN AND
methodsIn vitro phagocytosis of human or porcine primary islets or Min6 mouse insuloma cells by DCs was investigated by flow cytometry and confocal analysis. Subsequent innate DC responses were monitored by quantitative PCR and Western blotting of interferon-stimulated genes (ISGs).
resultsIn this study, we show that both mock- and coxsackievirus B3 (CVB3)-infected human and porcine pancreatic islets were efficiently phagocytosed by human monocyte-derived DCs. Phagocytosis of CVB3-infected, but not mock-infected, human and porcine islets resulted in induction of ISGs in DCs, including the retinoic acid-inducible gene (RIG)-I-like helicases (RLHs), RIG-I, and melanoma differentiation-associated gene 5 (Mda5). Studies with murine Min6 insuloma cells, which were also efficiently phagocytosed, revealed that increased ISG expression in DCs upon encountering CVB-infected cells resulted in an antiviral state that protected DCs from subsequent enterovirus infection. The observed innate antiviral responses depended on RNA within the phagocytosed cells, required endosomal acidification, and were type I interferon dependent.
conclusionsHuman DCs can phagocytose enterovirus-infected pancreatic cells and subsequently induce innate antiviral responses, such as induction of RLHs. These responses may have important consequences for immune homeostasis in vivo and may play a role in the etiology of type 1 diabetes.
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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.