ArticleDiabetes2013
Protection against type 1 diabetes upon Coxsackievirus B4 infection and iNKT-cell stimulation: role of suppressive macrophages.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Intestinal mucosal immunity and type 1 diabetes: Non-negligible communication between gut and pancreas.Diabetes, obesity & metabolism · 2025Review
- Changes in circulating NK and innate-like T cells in type 1 and type 2 diabetes.Frontiers in immunology · 2025Article
- Visualization of renal rotenone accumulation after oral administration andFrontiers in molecular biosciences · 2024Article
- Pathogenic analysis of coxsackievirus A10 in rhesus macaques.Virologica Sinica · 2022Article
- The iNKT Cell-Macrophage Axis in Homeostasis and Disease.International journal of molecular sciences · 2022Review
- The Kynurenine Pathway-New Linkage between Innate and Adaptive Immunity in Autoimmune Endocrinopathies.International journal of molecular sciences · 2021Review
- A Humanized Mouse Strain That Develops Spontaneously Immune-Mediated Diabetes.Frontiers in immunology · 2021Article
- Comprehensive Lipidome Profiling of the Kidney in Early-Stage Diabetic Nephropathy.Frontiers in endocrinology · 2020Article
- Monocytes and Macrophages as Viral Targets and Reservoirs.International journal of molecular sciences · 2018Review
- Targeting innate immunity to downmodulate adaptive immunity and reverse type 1 diabetes.ImmunoTargets and therapy · 2017Review
- Regulatory role of natural killer T cells in diabetes.Biomedical journal · 2015Review
- iNKT and MAIT Cell Alterations in Diabetes.Frontiers in immunology · 2015Review
Corrections and comments
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Authors and funding
8 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invariant natural killer T (iNKT) cells belong to the innate immune system and exercise a dual role as potent regulators of autoimmunity and participate in responses against different pathogens. They have been shown to prevent type 1 diabetes development and to promote antiviral responses. Many studies in the implication of environmental factors on the etiology of type 1 diabetes have suggested a link between enteroviral infections and the development of this disease. This study of the pancreatropic enterovirus Coxsackievirus B4 (CVB4) shows that although infection accelerated type 1 diabetes development in a subset of proinsulin 2-deficient NOD mice, the activation of iNKT cells by a specific agonist, α-galactosylceramide, at the time of infection inhibited the disease. Diabetes development was associated with the infiltration of pancreatic islets by inflammatory macrophages, producing high levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and activation of anti-islet T cells. On the contrary, macrophages infiltrating the islets after CVB4 infection and iNKT-cell stimulation expressed a number of suppressive enzymes, among which indoleamine 2,3-dioxygenase was sufficient to inhibit anti-islet T-cell response and to prevent diabetes. This study highlights the critical interaction between virus and the immune system in the acceleration or prevention of type 1 diabetes.
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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.