ArticlePloS one2013
1,25-Dihydroxyvitamin D3 suppresses TLR8 expression and TLR8-mediated inflammatory responses in monocytes in vitro and experimental autoimmune encephalomyelitis in vivo.
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 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Revealing the Mechanism of Buzhong Yiqi Tang in Ameliorating Autoimmune ThyroiditisCombinatorial chemistry & high throughput screening · 2026Article
- Mechanisms and Clinical Significance of Endosomal Toll-Like Receptors in Neurological Diseases.Molecular neurobiology · 2025Review
- Interaction between the non-alcoholic fatty liver disease fibrosis score and vitamin D deficiency on left ventricular hypertrophy and impaired diastolic function in patients with type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Optimizing serum 25(OH)D levels to mitigate the risk of age-related ocular diseases: insights from a large-scale prospective cohort study.Nutrition journal · 2025Article
- The Regulatory Effect of Vitamin D on Pancreatic Beta Cell Secretion in Patients with Type 2 Diabetes.Current medicinal chemistry · 2025Review
- Zika virus infection suppresses CYP24A1 and CAMP expression in human monocytes.Archives of virology · 2024Article
- Is there a window of opportunity for the therapeutic use of vitamin D in multiple sclerosis?Neural regeneration research · 2022Review
- Serum, Dietary, and Supplemental Vitamin D Levels and Insulin Resistance in 6294 Randomly Selected, Non-Diabetic U.S. Adults.Nutrients · 2022Article
- Distinct SARS-CoV-2 RNA fragments activate Toll-like receptors 7 and 8 and induce cytokine release from human macrophages and microglia.Frontiers in immunology · 2022Article
- RNA Sequencing of CD4Journal of molecular neuroscience : MN · 2021Article
- Lower peripheral blood Toll-like receptor 3 expression is associated with an unfavorable outcome in severe COVID-19 patients.Scientific reports · 2021Article
- Role of Toll-Like Receptors in Neuroimmune Diseases: Therapeutic Targets and Problems.Frontiers in immunology · 2021Review
- Vitamin D and Streptococci: The Interface of Nutrition, Host Immune Response, and Antimicrobial Activity in Response to Infection.ACS infectious diseases · 2020Review
- The Molecular Mechanisms by Which Vitamin D Prevents Insulin Resistance and Associated Disorders.International journal of molecular sciences · 2020Review
- Phase Angle: A Possible Biomarker to Quantify Inflammation in Subjects with Obesity and 25(OH)D Deficiency.Nutrients · 2019Observational
- Review
- Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis.Frontiers in molecular neuroscience · 2019Article
- Deficient arginase II expression without alteration in arginase I expression attenuated experimental autoimmune encephalomyelitis in mice.Immunology · 2018Article
- Protective Effect of 1,25-Dihydroxy Vitamin D3 on Pepsin-Trypsin-Resistant Gliadin-Induced Tight Junction Injuries.Digestive diseases and sciences · 2018Article
- Vitamin D, sub-inflammation and insulin resistance. A window on a potential role for the interaction between bone and glucose metabolism.Reviews in endocrine & metabolic disorders · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) suppresses autoimmunity and inflammation; however, the mechanism of its action has not been fully understood. We sought in this study to determine whether the anti-immune/anti-inflammatory action of 1,25(OH)2D3 is in part mediated through an interplay between 1,25(OH)2D3 and toll-like receptor (TLR)7/8 signaling. 1,25(OH)2D3 treatment prior to and/or following experimental autoimmune encephalomyelitis (EAE) induction effectively reduced inflammatory cytokine expression in the spinal cord and ameliorated EAE. These effects were accompanied with a reduction in expression of several TLRs with the most profound effect observed for TLR8. The expression of TLR8 adaptor protein MyD88 was also significantly reduced by 1,25(OH)2D3. To determine the molecular mechanism by which 1,25(OH)2D3 suppresses EAE induction of TLR8 and inflammatory cytokine expression, we evaluated whether 1,25(OH)2D3 can directly inhibit TLR8 signaling and the resulting inflammatory responses in human THP-1 monocytes. 1,25(OH)2D3 treatment not only significantly reduced TLR8 expression but also the expression or activity of MyD88, IRF-4, IRF-7 and NF-kB in monocytes challenged with TLR8 ligands. TLR8 promoter-luciferase reporter assays indicated that 1,25(OH)2D3 decreases TLR8 mRNA level in part via inhibiting TLR8 gene transcription activity. As a result of inhibition on TLR8 signaling cascade at various stages, 1,25(OH)2D3 significantly diminished the TLR8 target gene expression (TNF-α and IL-1β). In summary, our novel findings suggest that TLR8 is a new target of 1,25(OH)2D3 and may mediate the anti-inflammatory action of 1,25(OH)2D3. Our findings also point to a destructive role of TLR8 in EAE and shed lights on pathogenesis of multiple sclerosis.
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