ArticleScientific reports2019
Toll-like receptor 4 inhibition prevents autoimmune diabetes in NOD mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- 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
- The role of pancreatic islet macrophages in type 2 diabetes mellitus: from underlying pathological mechanisms to therapeutic target discovery.Metabolism open · 2025Review
- TRAF6 integrates innate immune signals to regulate glucose homeostasis via Parkin-dependent and Parkin-independent mitophagy.Science advances · 2025Article
- Toll Like Receptors Promote High Glucose-Induced Vascular Endothelial Cell Dysfunction by Regulating Neutrophil Extracellular Traps Formation.Inflammation · 2025Article
- Targeting innate immune sensors for therapeutic strategies in infectious diseases.Journal of microbiology (Seoul, Korea) · 2025Review
- Review
- Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice.NPJ biofilms and microbiomes · 2024Article
- Molecular Iodine Supplement Prevents Streptozotocin-Induced Pancreatic Alterations in Mice.Nutrients · 2022Article
- Isoflurane Attenuates Cerebral Ischaemia-Reperfusion Injury via the TLR4-NLRP3 Signalling Pathway in Diabetic Mice.Oxidative medicine and cellular longevity · 2022Article
- Toll-like Receptor 2 in Autoimmune Inflammation.Immune network · 2021Review
- Mining Helminths for Novel Therapeutics.Trends in molecular medicine · 2021Review
- Role of TLR4/MyD88/NF-κB signaling in heart and liver-related complications in a rat model of type 2 diabetes mellitus.The Journal of international medical research · 2021Article
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling.Cellular and molecular life sciences : CMLS · 2021Review
- A Strategy to Simultaneously Cure Type 1 Diabetes and Diabetic Nephropathy by Transplant of Composite Islet-Kidney Grafts.Frontiers in endocrinology · 2021Review
- Toll-like Receptors as a Potential Drug Target for Diabetes Mellitus and Diabetes-associated Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TLR4 is a transmembrane receptor of the innate immune system that recognizes LPS from gram-negative bacteria. Its stimulation induces pro-inflammatory responses and modulates adaptive immunity. Our aim is to determine the role of TLR4 in the activation and proliferation of T lymphocytes in the onset of autoimmune diabetes, using the non-obese diabetic (NOD) mouse model. Antigen-specific activation and proliferation of diabetogenic T cells were assessed in vitro by Carboxyfluorescein succinimidyl ester (CFSE) dilution, in presence of vehicle or CLI-095, a cyclohexene derivative that inhibits TLR4 signaling. NOD mice were treated with vehicle or CLI-095 and sacrificed either before or after the onset of autoimmune diabetes. T lymphocyte activation and proliferation were evaluated in treated and control mice. Insulitis was analyzed by histology and diabetes incidence was determined in treated and control mice. Our results demonstrate that TLR4 blockade decreases CD4+ T lymphocyte activation and auto-antigen-specific proliferation both in vitro and in vivo, decreases the infiltrative insulitis and finally prevents the onset of spontaneous diabetes. Taken together, our data demonstrate that TLR4 signaling contributes to the development and maintenance of autoimmune diabetes. The immunomodulatory effect of CLI-095 could be part of a preventive strategy targeting patients at risk for type 1 diabetes.
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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.