ArticleScientific reports2018
Comparative transcriptomic profile of tolerogenic dendritic cells differentiated with vitamin D3, dexamethasone and rapamycin.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- Synergistic immunomodulatory combinations induce robust human tolerogenic dendritic cells for antigen-specific regulatory T cell generation.The Journal of pharmacology and experimental therapeutics · 2026Article
- Rapamycin-modified novel tolerogenic dendritic cells induce liver graft tolerance through MHC-II+CD8+ regulatory T cells.Hepatology communications · 2026Article
- Restoring Immunological Tolerance via Dendritic Cells in Rheumatoid Arthritis.European journal of immunology · 2026Review
- Sustained microparticle-mediated intracellular immunomodulation enhances tolerogenic dendritic cell stability and antigen-specific Treg induction.Frontiers in immunology · 2026Article
- Leveraging current insights on IL-10-producing dendritic cells for developing effective immunotherapeutic approaches.FEBS letters · 2025Review
- Systemic rewiring of dendritic cells by melanoma-secreted midkine impairs immune surveillance and response to immune checkpoint blockade.Nature cancer · 2025Article
- Vitamin D as an Adjuvant Immune Enhancer to SARS-Cov-2 Vaccine.Current microbiology · 2025Article
- Human tolerogenic dendritic cell subtypes exert divergent effects on induction of cytotoxic CD4Frontiers in immunology · 2025Article
- Epigenetic signature of human vitamin D3 and IL-10 conditioned regulatory DCs.Scientific reports · 2024Article
- Peculiar transcriptional reprogramming with functional impairment of dendritic cells upon exposure to transformed HTLV-1-infected cells.PLoS pathogens · 2024Article
- Immuno-metabolic dendritic cell vaccine signatures associate with overall survival in vaccinated melanoma patients.Nature communications · 2023Article
- The Tolerogenic Influence of Dexamethasone on Dendritic Cells Is Accompanied by the Induction of Efferocytosis, Promoted by MERTK.International journal of molecular sciences · 2023Article
- The role of vitamin D in chronic obstructive pulmonary disease with pulmonary hypertension.Pulmonary circulation · 2023Article
- Aryl hydrocarbon receptor activity downstream of IL-10 signaling is required to promote regulatory functions in human dendritic cells.Cell reports · 2023Article
- Tolerogenic dendritic cells in type 1 diabetes: no longer a concept.Frontiers in immunology · 2023Review
- Review of potential medical treatments for middle ear cholesteatoma.Cell communication and signaling : CCS · 2022Review
- Distinct metabolic states guide maturation of inflammatory and tolerogenic dendritic cells.Nature communications · 2022Article
- Dendritic Cells and Their Immunotherapeutic Potential for Treating Type 1 Diabetes.International journal of molecular sciences · 2022Review
- Perioperative corticosteroid treatment impairs tumor-infiltrating dendritic cells in patients with newly diagnosed adult-type diffuse gliomas.Frontiers in immunology · 2022Article
- Dexamethasone treatment may mitigate adverse effects of vitamin D deficiency in hospitalized Covid-19 patients.Journal of medical virology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tolerogenic dendritic cell (tolDC)-based therapies have become a promising approach for the treatment of autoimmune diseases by their potential ability to restore immune tolerance in an antigen-specific manner. However, the broad variety of protocols used to generate tolDC in vitro and their functional and phenotypical heterogeneity are evidencing the need to find robust biomarkers as a key point towards their translation into the clinic, as well as better understanding the mechanisms involved in the induction of immune tolerance. With that aim, in this study we have compared the transcriptomic profile of tolDC induced with either vitamin D3 (vitD3-tolDC), dexamethasone (dexa-tolDC) or rapamycin (rapa-tolDC) through a microarray analysis in 5 healthy donors. The results evidenced that common differentially expressed genes could not be found for the three different tolDC protocols. However, individually, CYP24A1, MUCL1 and MAP7 for vitD3-tolDC; CD163, CCL18, C1QB and C1QC for dexa-tolDC; and CNGA1 and CYP7B1 for rapa-tolDC, constituted good candidate biomarkers for each respective cellular product. In addition, a further gene set enrichment analysis of the data revealed that dexa-tolDC and vitD3-tolDC share several immune regulatory and anti-inflammatory pathways, while rapa-tolDC seem to be playing a totally different role towards tolerance induction through a strong immunosuppression of their cellular processes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.