ArticleCellular and molecular life sciences : CMLS2020
Pancreatic beta cells persistently infected with coxsackievirus B4 are targets of NK cell-mediated cytolytic activity.
Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- Type 1 Diabetes Mellitus Pathogenesis: Mechanisms, Early Diagnostic Strategies, and Emerging Therapeutic Approaches.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Review
- Establishment of severe in vitro and in vivo infection models for coxsackievirus B4 and their application in identifying viral virulence determinants.Virologica Sinica · 2026Article
- Coxsackievirus B infection invokes unique cell-type-specific responses in primary human pancreatic islets.Cell reports · 2025Article
- Longitudinal Immune Profiling in Autoimmune Polyendocrine Syndrome Type 1.Scandinavian journal of immunology · 2025Article
- Immunogenicity and protective efficacy of inactivated coxsackievirus B4 viral particles.Emerging microbes & infections · 2024Article
- Coxsackievirus infection induces direct pancreatic β cell killing but poor antiviral CD8Science advances · 2024Article
- Review
- Lower percentages of natural killer cells in children with type 1 diabetes and their siblings.Pediatric endocrinology, diabetes, and metabolism · 2023Article
- Article
- Persistent coxsackievirus B infection and pathogenesis of type 1 diabetes mellitus.Nature reviews. Endocrinology · 2022Review
- Regulation of Pancreatic β-Cell Mass by Gene-Environment Interaction.Diabetes & metabolism journal · 2022Review
- Investigation of the utility of the 1.1B4 cell as a model human beta cell line for study of persistent enteroviral infection.Scientific reports · 2021Article
- Viruses and Type 1 Diabetes: From Enteroviruses to the Virome.Microorganisms · 2021Review
- Persistence of Coxsackievirus B4 in Pancreatic β Cells Disturbs Insulin Maturation, Pattern of Cellular Proteins, and DNA Methylation.Microorganisms · 2021Article
- Transcriptional networks in at-risk individuals identify signatures of type 1 diabetes progression.Science translational medicine · 2021Article
- Natural Killer Cells as Key Mediators in Type I Diabetes Immunopathology.Frontiers in immunology · 2021Review
- NK Cells in Autoimmune Diseases: Protective or Pathogenic?Frontiers in immunology · 2021Review
- Exploring the Triple Interaction between the Host Genome, the Epigenome, and the Gut Microbiome in Type 1 Diabetes.International journal of molecular sciences · 2020Review
- Structures and Functions of Viral 5' Non-Coding Genomic RNA Domain-I in Group-B Enterovirus Infections.Viruses · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
It has been suggested that the persistence of coxsackieviruses-B (CV-B) in pancreatic beta cells plays a role in the pathogenesis of type 1 diabetes (T1D). Yet, immunological effectors, especially natural killer (NK) cells, are supposed to clear virus-infected cells. Therefore, an evaluation of the response of NK cells to pancreatic beta cells persistently infected with CV-B4 was conducted. A persistent CV-B4 infection was established in 1.1B4 pancreatic beta cells. Infectious particles were found in supernatants throughout the culture period. The proportion of cells containing viral protein VP1 was low (< 5%), although a large proportion of cells harbored viral RNA (around 50%), whilst cell viability was preserved. HLA class I cell surface expression was downregulated in persistently infected cultures, but HLA class I mRNA levels were unchanged in comparison with mock-infected cells. The cytolytic activities of IL-2-activated non-adherent peripheral blood mononuclear cells (PBMCs) and of NK cells were higher towards persistently infected cells than towards mock-infected cells, as assessed by an LDH release assay. Impaired cytolytic activity of IL-2-activated non-adherent PBMCs from patients with T1D towards infected beta cells was observed. In conclusion, pancreatic beta cells persistently infected with CV-B4 can be lysed by NK cells, implying that impaired cytolytic activity of these effector cells may play a role in the persistence of CV-B in the host and thus in the viral pathogenesis of T1D.
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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.