ArticleEndocrinology2015
Toll-like receptor 3 is critical for coxsackievirus B4-induced type 1 diabetes in female NOD mice.
Article in Endocrinology, 2015. 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, 31 citations in OpenAlex.
- Toll-like receptor 3: a double-edged sword.Biomarker research · 2025Review
- Sensing danger in the islet: the roles of pattern recognition receptors in β cells and type 1 diabetes.Frontiers in immunology · 2025Review
- Immune repertoire profiling and T cell dysregulation in Peripheral Blood Mononuclear Cells of Type 2 diabetic patients.PloS one · 2025Article
- Coxsackievirus B Vaccines Prevent Infection-Accelerated Diabetes in NOD Mice and Have No Disease-Inducing Effect.Diabetes · 2021Article
- Consequences of Both Coxsackievirus B4 and Type 1 Diabetes on Female Non-Obese Diabetic Mouse Kidneys.Microorganisms · 2021Article
- Role of nucleic acid sensing in the pathogenesis of type 1 diabetes.World journal of diabetes · 2021Review
- A Humanized Mouse Strain That Develops Spontaneously Immune-Mediated Diabetes.Frontiers in immunology · 2021Article
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- Coxsackievirus B4 Exposure Results in Variable Pattern Recognition Response in the Kidneys of Female Non-Obese Diabetic Mice Before Establishment of Diabetes.Viral immunology · 2020Article
- Genetic Susceptibility of the Host in Virus-Induced Diabetes.Microorganisms · 2020Review
- Enteroviruses and T1D: Is It the Virus, the Genes or Both which Cause T1D.Microorganisms · 2020Review
- Norovirus Changes Susceptibility to Type 1 Diabetes by Altering Intestinal Microbiota and Immune Cell Functions.Frontiers in immunology · 2019Article
- TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells.Journal of autoimmunity · 2018Article
- Murine model of acute myocarditis and cerebral cortical neuron edema induced by coxsackievirus B4.Zoological research · 2018Article
- Modulation of the immune system by the gut microbiota in the development of type 1 diabetes.Human vaccines & immunotherapeutics · 2018Article
- Article
- Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset.Frontiers in endocrinology · 2017Review
- The Four-Way Stop Sign: Viruses, 12-Lipoxygenase, Islets, and Natural Killer Cells in Type 1 Diabetes Progression.Frontiers in endocrinology · 2017Article
- Article
- The role of the innate immune system in destruction of pancreatic beta cells in NOD mice and humans with type I diabetes.Journal of autoimmunity · 2016Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Group B coxsackieviruses (CVBs) are involved in triggering some cases of type 1 diabetes mellitus (T1DM). However, the molecular mechanism(s) responsible for this remain elusive. Toll-like receptor 3 (TLR3), a receptor that recognizes viral double-stranded RNA, is hypothesized to play a role in virus-induced T1DM, although this hypothesis is yet to be substantiated. The objective of this study was to directly investigate the role of TLR3 in CVB-triggered T1DM in nonobese diabetic (NOD) mice, a mouse model of human T1DM that is widely used to study both spontaneous autoimmune and viral-induced T1DM. As such, we infected female wild-type (TLR3(+/+)) and TLR3 knockout (TLR3(-/-)) NOD mice with CVB4 and compared the incidence of diabetes in CVB4-infected mice with that of uninfected counterparts. We also evaluated the islets of uninfected and CVB4-infected wild-type and TLR3 knockout NOD mice by immunohistochemistry and insulitis scoring. TLR3 knockout mice were markedly protected from CVB4-induced diabetes compared with CVB4-infected wild-type mice. CVB4-induced T-lymphocyte-mediated insulitis was also significantly less severe in TLR3 knockout mice compared with wild-type mice. No differences in insulitis were observed between uninfected animals, either wild-type or TLR3 knockout mice. These data demonstrate for the first time that TLR3 is 1) critical for CVB4-induced T1DM, and 2) modulates CVB4-induced insulitis in genetically prone NOD mice.
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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.