ArticleExperimental & molecular medicine2012
Toll-like receptor 4 on islet β cells senses expression changes in high-mobility group box 1 and contributes to the initiation of type 1 diabetes.
Article in Experimental & molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Metabolic abnormalities and obesity's impact on the risk for developing preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Pooled it
- Toll Like Receptor 4: A Potential Link Between Obesity and Metabolic Diseases.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Dendritic Cells as Immunometabolic Regulatory Nodes in Diabetes: Molecular Mechanisms and Therapeutic Reprogramming.International journal of molecular sciences · 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
- Investigating the protective effect of zinc supplementation on streptozotocin-induced pancreatic beta-cell damage via the HMGB1/TLR2/MAPK pathway.Iranian journal of basic medical sciences · 2026Article
- Inhibition of the TLR4/RAGE pathway by clearance of extracellular HMGB1 is a potential therapeutic target for radiation-damaged salivary glands.Regenerative therapy · 2025Article
- Integrating machine learning and bioinformatics approaches to identify novel diagnostic gene biomarkers for diabetic mice.Scientific reports · 2025Article
- Sensing danger in the islet: the roles of pattern recognition receptors in β cells and type 1 diabetes.Frontiers in immunology · 2025Review
- Article
- Advancements in innate immune regulation strategies in islet transplantation.Frontiers in immunology · 2023Review
- How do parasitic worms prevent diabetes? An exploration of their influence on macrophage and β-cell crosstalk.Frontiers in endocrinology · 2023Review
- Protective effect of dexmedetomidine on intestinal mucosal barrier function in rats after cardiopulmonary bypass.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- HMGB1 as a therapeutic target in disease.Journal of cellular physiology · 2021Review
- Toll-like receptor 7 deficiency suppresses type 1 diabetes development by modulating B-cell differentiation and function.Cellular & molecular immunology · 2021Article
- Long-term inhibition of dipeptidyl-peptidase 4 reduces islet infiltration and downregulates IL-1β and IL-12 in NOD mice.International immunopharmacology · 2020Article
- Effects of 1,25-dihydroxyvitamin D3 on the Inflammatory Responses of Stromal Vascular Cells and Adipocytes from Lean and Obese Mice.Nutrients · 2020Article
- Fucoidan prevent murine autoimmune diabetes via suppression TLR4-signaling pathways, regulation DC/Treg induced immune tolerance and improving gut microecology.Nutrition & metabolism · 2019Article
- Ethyl Pyruvate Stimulates Regulatory T Cells and Ameliorates Type 1 Diabetes Development in Mice.Frontiers in immunology · 2018Article
- New application of anti-TLR monoclonal antibodies: detection, inhibition and protection.Inflammation and regeneration · 2018Review
- An ancestral retroviral protein identified as a therapeutic target in type-1 diabetes.JCI insight · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes mellitus is caused by the autoimmune destruction of β cells within the islets. In recent years, innate immunity has been proposed to play a key role in this process. High-mobility group box 1 (HMGB1), an inflammatory trigger in a number of autoimmune diseases, activates proinflammatory responses following its release from necrotic cells. Our aim was to determine the significance of HMGB1 in the natural history of diabetes in non-obese diabetic (NOD) mice. We observed that the rate of HMGB1 expression in the cytoplasm of islets was much greater in diabetic mice compared with non-diabetic mice. The majority of cells positively stained for toll-like receptor 4 (TLR4) were β cells; few α cells were stained for TLR4. Thus, we examined the effects of anti-TLR4 antibodies on HMGB1 cell surface binding, which confirmed that HMGB1 interacts with TLR4 in isolated islets. Expression changes in HMGB1 and TLR4 were detected throughout the course of diabetes. Our findings indicate that TLR4 is the main receptor on β cells and that HMGB1 may signal via TLR4 to selectively damage β cells rather than α cells during the development of type 1 diabetes mellitus.
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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.