ArticleScientific reports2016
Incomplete immune response to coxsackie B viruses associates with early autoimmunity against insulin.
Article in Scientific reports, 2016. 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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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Coxsackievirus B escapes antiviral CD8Science advances · 2026Article
- Coxsackie B1 virus-like particle vaccine modified to exclude a highly conserved immunoreactive region from the capsid induces potent neutralizing antibodies and protects against infection in mice.Journal of biomedical science · 2025Article
- Joint analysis of the nPOD-Virus Group data: the association of enterovirus with type 1 diabetes is supported by multiple markers of infection in pancreas tissue.Diabetologia · 2025Article
- The perfect storm: unraveling the interplay of genetic predisposition and viral triggers in type 1 diabetes pathogenesis.Frontiers in endocrinology · 2025Review
- Clonal associations between lymphocyte subsets and functional states in rheumatoid arthritis synovium.Nature communications · 2024Article
- Coxsackievirus infection induces direct pancreatic β cell killing but poor antiviral CD8Science advances · 2024Article
- Tracking DNA-based antigen-specific T cell receptors during progression to type 1 diabetes.Science advances · 2023Article
- Distinct transcriptomic profiles in children prior to the appearance of type 1 diabetes-linked islet autoantibodies and following enterovirus infection.Nature communications · 2023Article
- The countdown to type 1 diabetes: when, how and why does the clock start?Diabetologia · 2023Review
- The protective roles of allicin on type 1 diabetes mellitus through AMPK/mTOR mediated autophagy pathway.Frontiers in pharmacology · 2023Article
- Enteroviruses and Type 1 Diabetes: Multiple Mechanisms and Factors?Annual review of medicine · 2022Review
- A Public Health Antibody Screening Indicates a 6-Fold Higher SARS-CoV-2 Exposure Rate than Reported Cases in Children.Med (New York, N.Y.) · 2021Article
- Using the T Cell Receptor as a Biomarker in Type 1 Diabetes.Frontiers in immunology · 2021Review
- Neoepitopes in Type 1 Diabetes: Etiological Insights, Biomarkers and Therapeutic Targets.Frontiers in immunology · 2021Article
- Virus Infection Is an Instigator of Intestinal Dysbiosis Leading to Type 1 Diabetes.Frontiers in immunology · 2021Review
- Type 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infection.Microorganisms · 2020Review
- Why is the presence of autoantibodies against GAD associated with a relatively slow progression to clinical diabetes?Diabetologia · 2020Article
- Innate Viral Sensor MDA5 and Coxsackievirus Interplay in Type 1 Diabetes Development.Microorganisms · 2020Review
- Current understandings of the pathogenesis of type 1 diabetes: Genetics to environment.World journal of diabetes · 2020Review
- Rationale for enteroviral vaccination and antiviral therapies in human type 1 diabetes.Diabetologia · 2019Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral infections are associated with autoimmunity in type 1 diabetes. Here, we asked whether this association could be explained by variations in host immune response to a putative type 1 etiological factor, namely coxsackie B viruses (CVB). Heterogeneous antibody responses were observed against CVB capsid proteins. Heterogeneity was largely defined by different binding to VP1 or VP2. Antibody responses that were anti-VP2 competent but anti-VP1 deficient were unable to neutralize CVB, and were characteristic of children who developed early insulin-targeting autoimmunity, suggesting an impaired ability to clear CVB in early childhood. In contrast, children who developed a GAD-targeting autoimmunity had robust VP1 and VP2 antibody responses to CVB. We further found that 20% of memory CD4(+) T cells responding to the GAD65247-266 peptide share identical T cell receptors to T cells responding to the CVB4 p2C30-51 peptide, thereby providing direct evidence for the potential of molecular mimicry as a mechanism for GAD autoimmunity. Here, we highlight functional immune response differences between children who develop insulin-targeting and GAD-targeting autoimmunity, and suggest that children who lose B cell tolerance to insulin within the first years of life have a paradoxical impaired ability to mount humoral immune responses to coxsackie viruses.
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