ArticleThe Journal of clinical investigation2024
Targeting aryl hydrocarbon receptor functionally restores tolerogenic dendritic cells derived from patients with multiple sclerosis.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Mechanistic Insights into Regulation of the Aryl Hydrocarbon Receptor Expression in Mouse and Human Hepatoma Cells.International journal of molecular sciences · 2026Article
- Tolerogenic dendritic cell-conditioned medium promotes hair growth by modulating follicular microenvironment in a DHT-treated mouse model.Molecular and cellular biochemistry · 2026Article
- Lactobacillus plantarum-derived indole-3-lactic acid inhibits prostate cancer progression through ASF1B/ENO1 axis and remodels the tumor microenvironment to enhance anti-PD-1 therapy.Molecular biomedicine · 2026Article
- Synergistic immunomodulatory combinations induce robust human tolerogenic dendritic cells for antigen-specific regulatory T cell generation.The Journal of pharmacology and experimental therapeutics · 2026Article
- Assessing the Early Economic Feasibility of a Curative Gene Therapy for Multiple Sclerosis Using a Risk-Adjusted Valuation Framework.Healthcare (Basel, Switzerland) · 2026Article
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
- Cellular Immunotherapies for Multiple Sclerosis: Mechanistic Insights and Clinical Advances.International journal of molecular sciences · 2026Review
- Gene expression profiling of dendritic cell tolerance dysfunction in women with systemic lupus erythematosus.Frontiers in immunology · 2026Article
- Interferon-γ-induced tolerogenic dendritic cells ameliorate autoimmune neuroinflammation and suppress T-cell responses in multiple sclerosis.Frontiers in immunology · 2026Article
- Identification and Preliminary mRNA Validation of Key Genes Associated with Tolerogenic Dendritic Cells in Keloid Based on Transcriptome Data.Clinical, cosmetic and investigational dermatology · 2026Article
- Plant defense-directed discovery of a natural anti-psoriasis agent targeting GAPDH.Science advances · 2025Article
- Human tolerogenic dendritic cell subtypes exert divergent effects on induction of cytotoxic CD4Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic disease characterized by dysregulated self-reactive immune responses that damage the neurons' myelin sheath, leading to progressive disability. The primary therapeutic option, immunosuppressants, inhibits pathogenic anti-myelin responses but depresses the immune system. Antigen-specific monocyte-derived autologous tolerogenic dendritic cells (tolDCs) offer alternative therapeutic approaches to restore tolerance to autoantigens without causing generalized immunosuppression. However, immune dysregulation in MS could impact the properties of the monocytes used as starting material for this cell therapy. Here, we characterized CD14+ monocytes, mature dendritic cells, and vitamin D3-tolDCs (VitD3-tolDCs) from active, treatment-naive MS patients and healthy donors (HDs). Using multiomics, we identified a switch in these cell types toward proinflammatory features characterized by alterations in the aryl hydrocarbon receptor (AhR) and NF-κB pathways. MS patient-derived VitD3-tolDCs showed reduced tolerogenic properties compared with those from HDs, which were fully restored through direct AhR agonism and by use of in vivo or in vitro dimethyl fumarate (DMF) supplementation. Additionally, in the experimental autoimmune encephalomyelitis mouse model, combined therapy of DMF and VitD3-tolDCs was more efficient than monotherapies in reducing the clinical score of mice. We propose that a combined therapy with DMF and VitD3-tolDCs offers enhanced therapeutic potential in treating MS.
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