ArticlePloS one2013
Toll-like receptor 4 deficiency accelerates the development of insulin-deficient diabetes in non-obese diabetic mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 64 citations in OpenAlex.
- Taking its TOLL: the role of toll-like receptor 4 in human health and disease, and its potential as a therapeutic target.Frontiers in immunology · 2026Review
- Modulating Metabolic Health and Physiological Functions: Advances in Dietary Interventions Targeting Gut Microbiota.Therapeutics and clinical risk management · 2025Review
- Sensing danger in the islet: the roles of pattern recognition receptors in β cells and type 1 diabetes.Frontiers in immunology · 2025Review
- Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice.NPJ biofilms and microbiomes · 2024Article
- TLR5-deficiency controls dendritic cell subset development in an autoimmune diabetes-susceptible model.Frontiers in immunology · 2024Article
- Metabolic Syndrome: A Narrative Review from the Oxidative Stress to the Management of Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Gut Microbiota Is Associated with Onset and Severity of Type 1 Diabetes in Nonobese Diabetic Mice Treated with Anti-PD-1.ImmunoHorizons · 2023Article
- Article
- Microbiota in health and diseases.Signal transduction and targeted therapy · 2022Review
- A bridge for short-chain fatty acids to affect inflammatory bowel disease, type 1 diabetes, and non-alcoholic fatty liver disease positively: by changing gut barrier.European journal of nutrition · 2021Review
- Dysbiosis in the Development of Type I Diabetes and Associated Complications: From Mechanisms to Targeted Gut Microbes Manipulation Therapies.International journal of molecular sciences · 2021Review
- Toll-like receptor 7 deficiency suppresses type 1 diabetes development by modulating B-cell differentiation and function.Cellular & molecular immunology · 2021Article
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- Lipid deposition and metaflammation in diabetic kidney disease.Current opinion in pharmacology · 2020Review
- Distinct alterations of gut morphology and microbiota characterize accelerated diabetes onset in nonobese diabetic mice.The Journal of biological chemistry · 2020Article
- The Role of Gut Microbiota and Environmental Factors in Type 1 Diabetes Pathogenesis.Frontiers in endocrinology · 2020Review
- Evaluating the Causal Role of Gut Microbiota in Type 1 Diabetes and Its Possible Pathogenic Mechanisms.Frontiers in endocrinology · 2020Review
- Revisiting the Hygiene Hypothesis in the Context of Autoimmunity.Frontiers in immunology · 2020Review
- Toll-like receptor 4 inhibition prevents autoimmune diabetes in NOD mice.Scientific reports · 2019Article
- Targeting Type 1 Diabetes: Selective Approaches for New Therapies.Biochemistry · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveToll-like receptors (TLR) mediate the recognition of microbial constituents and stress-induced endogenous ligands by the immune system. They may also be involved in the maintenance or break down of tolerance against autologous antigens. The aim of our investigation was to study the consequence of TLR4 deficiency on the development of insulin-deficient diabetes in the NOD mouse.
methodsThe TLR4 defect of the C57BL/10ScN mouse was backcrossed onto the NOD background and the effect of TLR4 deficiency on diabetes development was analysed by in vivo and in vitro studies.
resultsCompared to animals with wildtype TLR4 expression (TLR4(+/+)), female NOD mice carrying a homozygous TLR4 defect (TLR4(-/-)), showed significant acceleration of diabetes development, with a younger age at diabetes onset (TLR4 (+/+) 177±22 d, TLR(-/-): 118±21 d; p<0.01). Pancreata of 120 d old TLR4(-/-) NOD mice revealed increased proportions of islets with advanced stages of immune cell infiltration compared to TLR4(+/+) mice (p<0.05). TLR4 deficiency did not affect the susceptibility of islet cells to the beta cell damaging mediators nitric oxide or the inflammatory cytokines tumor necrosis factor alpha, interleukin-1 beta and interferon gamma. The lack of TLR4 further had no effect on the frequency of regulatory T-cells but reduced their capacity to inhibit T-cell proliferation.
conclusionsOur findings demonstrate that TLR4 deficiency results in an acceleration of diabetes development and immune cell infiltration of islets in NOD mice. We conclude that TLR4 is involved in the progression of the insulitis process thereby controlling the development of insulin-deficient diabetes in NOD mice.
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