ArticleJournal of virology2013
Induction of an antiviral state and attenuated coxsackievirus replication in type III interferon-treated primary human pancreatic islets.
Article in Journal of virology, 2013. 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, 43 citations in OpenAlex.
- Transcriptomic characterization of human pancreatic CD206- and CD206 + macrophages.Scientific reports · 2025Article
- Circulating Sphingolipids in Insulin Resistance, Diabetes and Associated Complications.International journal of molecular sciences · 2023Review
- The role of the interferon/JAK-STAT axis in driving islet HLA-I hyperexpression in type 1 diabetes.Frontiers in endocrinology · 2023Review
- Temporal regulation of interferon signalling in human EndoC-βH1 cells.Journal of molecular endocrinology · 2022Article
- Persistent coxsackievirus B1 infection triggers extensive changes in the transcriptome of human pancreatic ductal cells.iScience · 2022Article
- Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells-A Strategy Used by Coxsackie B Virus to Evade the Host's Innate Immune Response at the Primary Site of Infection?Microorganisms · 2021Article
- Type 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infection.Microorganisms · 2020Review
- Review
- Innate Viral Sensor MDA5 and Coxsackievirus Interplay in Type 1 Diabetes Development.Microorganisms · 2020Review
- Molecular Pathogenicity of Enteroviruses Causing Neurological Disease.Frontiers in microbiology · 2020Review
- Coxsackievirus B Persistence Modifies the Proteome and the Secretome of Pancreatic Ductal Cells.iScience · 2019Article
- Enteroviral infections in the pathogenesis of type 1 diabetes: new insights for therapeutic intervention.Current opinion in pharmacology · 2018Review
- Potential role of type I interferon in the pathogenic process leading to type 1 diabetes.Current opinion in endocrinology, diabetes, and obesity · 2018Review
- A Link Between a Common Mutation in CFTR and Impaired Innate and Adaptive Viral Defense.The Journal of infectious diseases · 2017Article
- Diabetes, the TYK2 Gene and the Interferon Response: In Search for Environmental Causes.EBioMedicine · 2017Article
- The innate immune receptor MDA5 limits rotavirus infection but promotes cell death and pancreatic inflammation.The EMBO journal · 2017Article
- Interferon-α mediates human beta cell HLA class I overexpression, endoplasmic reticulum stress and apoptosis, three hallmarks of early human type 1 diabetes.Diabetologia · 2017Article
- Characterization of resident lymphocytes in human pancreatic islets.Clinical and experimental immunology · 2017Article
- An IFIH1 gene polymorphism associated with risk for autoimmunity regulates canonical antiviral defence pathways in Coxsackievirus infected human pancreatic islets.Scientific reports · 2016Article
- Enteroviral proteases: structure, host interactions and pathogenicity.Reviews in medical virology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Type III interferons (IFNs), also called lambda interferons (IFN-λ), comprise three isoforms, IFN-λ1 (interleukin-29 [IL-29]), IFN-λ2 (IL-28A), and IFN-λ3 (IL-28B). Only limited information is available on their expression and biological functions in humans. Type I and type II IFNs protect human pancreatic islets against coxsackievirus infection, and this is important since such viruses have been proposed to play a role in the development of human type 1 diabetes. Here we investigated whether type III IFN is expressed during infection of human islet cells with coxsackievirus and if type III IFN regulates permissiveness to such infections. We show that human islets respond to a coxsackievirus serotype B3 (CVB3) infection by inducing the expression of type III IFNs. We also demonstrate that islet endocrine cells from nondiabetic individuals express the type III IFN receptor subunits IFN-λR1 and IL-10R2. Pancreatic alpha cells express both receptor subunits, while pancreatic beta cells express only IL-10R2. Type III IFN stimulation elicited a biological response in human islets as indicated by the upregulated expression of antiviral genes as well as pattern recognition receptors. We also show that type III IFN significantly reduces CVB3 replication. Our studies reveal that type III IFNs are expressed during CVB3 infection and that the expression of the type III IFN receptor by the human pancreatic islet allows this group of IFNs to regulate the islets' permissiveness to infection. Our novel observations suggest that type III IFNs may regulate viral replication and thereby contribute to reduced tissue damage and promote islet cell survival during coxsackievirus infection.
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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.