ArticleScientific reports2016
Rotavirus acceleration of type 1 diabetes in non-obese diabetic mice depends on type I interferon signalling.
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 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Multi-tissue multi-omics integration reveals tissue-specific pathways, gene networks and drug candidates for type 1 diabetes.Diabetologia · 2026Article
- Viruses as a potential environmental trigger of type 1 diabetes mellitus (Review).Biomedical reports · 2024Review
- Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice.NPJ biofilms and microbiomes · 2024Article
- Review
- Evidence Suggesting the Role of Gut Dysbiosis in Diabetic Retinopathy.Investigative ophthalmology & visual science · 2022Review
- The dark side of the gut: Virome-host interactions in intestinal homeostasis and disease.The Journal of experimental medicine · 2021Review
- Virus Infection Is an Instigator of Intestinal Dysbiosis Leading to Type 1 Diabetes.Frontiers in immunology · 2021Review
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- Gut eukaryotic virome in colorectal carcinogenesis: Is that a trigger?Computational and structural biotechnology journal · 2021Review
- Rotavirus and Type 1 Diabetes-Is There a Connection? A Synthesis of the Evidence.The Journal of infectious diseases · 2020Review
- Genetic Susceptibility of the Host in Virus-Induced Diabetes.Microorganisms · 2020Review
- Norovirus Changes Susceptibility to Type 1 Diabetes by Altering Intestinal Microbiota and Immune Cell Functions.Frontiers in immunology · 2019Article
- Rotavirus infection beyond the gut.Infection and drug resistance · 2019Review
- The Intestinal Virome and Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- MHC class I expression in intestinal cells is reduced by rotavirus infection and increased in bystander cells lacking rotavirus antigen.Scientific reports · 2018Article
- Exercise Training but not Curcumin Supplementation Decreases Immune Cell Infiltration in the Pancreatic Islets of a Genetically Susceptible Model of Type 1 Diabetes.Sports medicine - open · 2017Article
- Rotavirus infection.Nature reviews. Disease primers · 2017Review
- Isogenic Cellular Systems Model the Impact of Genetic Risk Variants in the Pathogenesis of Type 1 Diabetes.Frontiers in endocrinology · 2017Review
- A Pre-Clinical Safety Evaluation of SBP (HBsAg-Binding Protein) Adjuvant for Hepatitis B Vaccine.PloS one · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rotavirus infection is associated with childhood progression to type 1 diabetes. Infection by monkey rotavirus RRV accelerates diabetes onset in non-obese diabetic (NOD) mice, which relates to regional lymph node infection and a T helper 1-specific immune response. When stimulated ex vivo with RRV, plasmacytoid dendritic cells (pDCs) from naïve NOD mice secrete type I interferon, which induces the activation of bystander lymphocytes, including islet-autoreactive T cells. This is our proposed mechanism for diabetes acceleration by rotaviruses. Here we demonstrate bystander lymphocyte activation in RRV-infected NOD mice, which showed pDC activation and strong upregulation of interferon-dependent gene expression, particularly within lymph nodes. The requirement for type I interferon signalling was analysed using NOD mice lacking a functional type I interferon receptor (NOD.IFNAR1(-/-) mice). Compared with NOD mice, NOD.IFNAR1(-/-) mice showed 8-fold higher RRV titers in lymph nodes and 3-fold higher titers of total RRV antibody in serum. However, RRV-infected NOD.IFNAR1(-/-) mice exhibited delayed pDC and lymphocyte activation, no T helper 1 bias in RRV-specific antibodies and unaltered diabetes onset when compared with uninfected controls. Thus, the type I interferon signalling induced by RRV infection is required for bystander lymphocyte activation and accelerated type 1 diabetes onset in genetically susceptible mice.
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