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RNA-seq analysis of human T CD4+ cells after their interaction with autologous antigen-specific vitamin D3-generated tolerogenic dendritic cells

ABSTRACT: RNA-seq analysis of human T CD4+ cells after their interaction with autologous antigen-specific vitamin D3-generated tolerogenic dendritic cells

PROVIDER: PRJNA528946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8782810_1.fastq.gz	Fastqsanger.gz
	SRR8782810_2.fastq.gz	Fastqsanger.gz
	SRR8782820_1.fastq.gz	Fastqsanger.gz
	SRR8782820_2.fastq.gz	Fastqsanger.gz
	SRR8782801_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of human T CD4+ cells after their interaction with autologous antigen-specific vitamin D3-generated tolerogenic dendritic cells

Project description:The use of autologous tolerogenic dendritic cells (tolDC) has become a promising alternative for the treatment of autoimmune diseases. Among the different alternatives available, the use of vitamin D3 for the generation of tolDC (vitD3‑tolDC) constitutes one of the most robust approaches due to their immune regulatory properties, which are currently being tested in clinical trials. However, the mechanisms that vitD3‑tolDC are triggering for the induction of tolerance remain elusive. For this reason, we have performed a full transcriptomic characterization of T cells upon their interaction with autologous, antigen-specific vitD3-tolDC. Our results evidenced a strong down-modulation of genes involved in cell cycle and cell response to immune-related stimuli in T CD4+ cells after their interaction with vitD3-tolDC. Consequently, our results show the induction of a strong antigen-specific hyporresponsiveness, which manifests the regulatory properties of these cells and therefore their therapeutic potential in the clinic.

2020-12-21 | GSE128816 | GEO

Microarray of tolerogenic dendritic cells differentiated in the presence of vitamin D3, dexamethasone or rapamycin

Project description:The comparative analysis of the transcriptome of tolerogenic dendritic cells (tolDC) differentiated using different stimulus (either vitamin D3, dexamethasone or rapamycin) would allow to evidence potential common genes and pathways that could explain their potency as tolerance-inducing cells.

2018-07-31 | E-MTAB-6937 | biostudies-arrayexpress

Dimethyl Fumarate Restores Functional Vitamin-D3 Tolerogenic Dendritic Cells differentiated from Multiple Sclerosis Patients

Project description:Multiple Sclerosis (MS) is a chronic disease characterised by dysregulated self-reactive immune responses damaging neurons’ myelin sheath, causing disability. The primary therapeutic option, immunosuppressants, inhibit pathogenic anti-myelin responses but depresses the entire immune system. Antigen-specific autologous tolerogenic dendritic cell (tolDC) therapies offer an approach to restore tolerance to auto-antigens without causing generalised immunosuppression. However, immune dysregulation in MS could impact the phenotype and functionality of the starting material for cell therapy. In this study, we defined the immune signature of CD14+ monocytes, mature dendritic cells (mDCs) and Vitamin D3 tolDCs (VitD3-tolDCs) isolated from MS patients and healthy donors (HD). By using a multi-omic approach, we identified a shift in these cell types toward a proinflammatory profile dominated by alterations in the AhR pathway and increased NFkB signalling. Moreover, tolDCs isolated from MS patients showed reduced tolerogenic properties compared to those from HD, which were fully restored through AhR agonism and NFkB downregulation through in vivo or in vitro supplementation with Dimethyl Fumarate (DMF). Remarkably, a combined therapy of DMF and VitD3-tolDC was more efficient to reduce the clinical score of experimental autoimmune encephalomyelitis mice than monotherapies. In summary, we demonstrate that DMF restores the functionality of VitD3-tolDCs derived from MS patients. Moreover, a combined therapy with DMF and VitD3-tolDCs could offer enhanced therapeutic potential in treating MS.

2024-12-13 | GSE267576 | GEO

Dimethyl Fumarate Restores Functional Vitamin-D3 Tolerogenic Dendritic Cells differentiated from Multiple Sclerosis Patients [Methylation_array]

2024-12-13 | GSE267660 | GEO

Transcriptome profiling of gingival fibroblasts treated by vitamin D3

Project description:In humans, vitamin D3 is a secosteroid, a prohormonal precursor of biologically active hydroxyforms. Vitamin D3 is related to periodontitis. The third American Health and Nutrition Survey found that plasma 25(OH)D3 levels are negatively correlated with attachment loss in people aged >50 years. The relationship between vitamin D3 and periodontitis remains to be investigated. We sent human gingival fibroblasts treated by vitamin D3 for transcriptome sequencing.

2022-09-09 | GSE212728 | GEO

Dimethyl Fumarate Restores Functional Vitamin-D3 Tolerogenic Dendritic Cells differentiated from Multiple Sclerosis Patients

Project description:Dimethyl Fumarate Restores Functional Vitamin-D3 Tolerogenic Dendritic Cells differentiated from Multiple Sclerosis Patients

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Dimethyl Fumarate Restores Functional Vitamin-D3 Tolerogenic Dendritic Cells differentiated from Multiple Sclerosis Patients [Methylation_array]

Project description:Dimethyl Fumarate Restores Functional Vitamin-D3 Tolerogenic Dendritic Cells differentiated from Multiple Sclerosis Patients [Methylation_array]

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Expression array analysis of the effects of vitamin D3 and mutp53

Project description:We wanted to examine the effect of vitamin D3 and endogenous mutant p53 expressed in SKBR3 cells on gene expression paterns. Expression microarray analysis was performed on SKBR3 cells without or with endogenous mutp53 knockdown, with or without 1a25-vitamin D3 treatment.

2009-12-29 | GSE19670 | GEO

Vitamin D3 and deconvoluting a rash

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Vitamin D Receptor (VDR) ChIP-seq reported in "Vitamin D receptor and STAT3 cooperate to TET2-mediated acquisition of tolerogenesis"

Project description:The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), induces stable tolerogenesis in dendritic cells (DC). This process involves the Vitamin D receptor (VDR) which translocates to the nucleus, binds its cognate genomic sites and promotes epigenetic and transcriptional remodeling. In this study, we investigated the interplay between the vitamin D receptor (VDR) and transcription factors to induce DNA methylation changes, which might provide phenotypic stability to the tolerogenic phenotype of DCs.

2022-02-23 | GSE145584 | GEO

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