Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Autocrine vitamin D signaling switches off pro-inflammatory programs of Th1 cells

ABSTRACT: Autocrine vitamin D signaling switches off pro-inflammatory programs of Th1 cells

PROVIDER: PRJNA647352 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12267560.fastq.gz	Fastqsanger.gz
	SRR12267561.fastq.gz	Fastqsanger.gz
	SRR12267562.fastq.gz	Fastqsanger.gz
	SRR12267563.fastq.gz	Fastqsanger.gz
	SRR12267564.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 75

Similar Datasets

Autocrine vitamin D signaling switches off pro-inflammatory programs of Th1 cells

Project description:The molecular mechanisms governing orderly shutdown and retraction of CD4+ T helper (Th)1 responses remain poorly understood. Here, we show that complement triggers contraction of Th1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor (VDR) and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated transition from pro-inflammatory IFN-γ+ Th1 cells to suppressive IL-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VDR shaped the transcriptional response to VitD. Accordingly, VitD did not induce IL-10 in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of COVID-19 patients were Th1-skewed and showed de-repression of genes down-regulated by VitD, either from lack of substrate (VitD deficiency) and/or abnormal regulation of this system.

2021-10-19 | GSE154741 | GEO

Autocrine vitamin D signaling switches off pro-inflammatory programs of T<sub>H</sub>1 cells.

Project description:The molecular mechanisms governing orderly shutdown and retraction of CD4+ type 1 helper T (TH1) cell responses remain poorly understood. Here we show that complement triggers contraction of TH1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ+ TH1 cells to suppressive interleukin-10+ cells. This process was primed by dynamic changes in the epigenetic landscape of CD4+ T cells, generating super-enhancers and recruiting several transcription factors, notably c-JUN, STAT3 and BACH2, which together with VitD receptor shaped the transcriptional response to VitD. Accordingly, VitD did not induce interleukin-10 expression in cells with dysfunctional BACH2 or STAT3. Bronchoalveolar lavage fluid CD4+ T cells of patients with COVID-19 were TH1-skewed and showed de-repression of genes downregulated by VitD, from either lack of substrate (VitD deficiency) and/or abnormal regulation of this system.

| S-EPMC7612139 | biostudies-literature

A male infertility mutation switches NANOS1 activity from anti-apoptotic to pro-apoptotic

Project description:A male infertility mutation switches NANOS1 activity from anti-apoptotic to pro-apoptotic

| PRJNA557689 | ENA

Pro-oxidant therapy by a vitamin K precursor targets PI 3-Kinase VPS34 function

Project description:Men taking anti-oxidant vitamin E supplements have increased prostate cancer (PC) risk. Whether pro- oxidants protect from PC remained unclear. We show that a pro-oxidant vitamin K precursor (MSB) suppresses PC progression in mice killing cells through an oxidative cell death: MSB antagonizes the essential class III PI 3-Kinase VPS34 the regulator of endosome identity and sorting through oxidation of key cysteines pointing to a redox checkpoint in sorting. Testing MSB in a myotubular myopathy model that is driven by loss of MTM1 the phosphatase antagonist of VPS34 we show that dietary MSB improved muscle histology function and extended life span. These findings enhance our understanding of pro-oxidant selectivity and show how definition of the pathways they impinge on can give rise to unexpected therapeutic opportunities.

2024-04-02 | GSE148011 | GEO

Effect of cathepsin inhibitors in signals associated with Th1 and Th2 mediators by Dendritic Cells

Project description:Cathepsin inhibitors have been associated to induce changes in Th1/Th2 polarization; cathepsin B inhibitor CA074 has been reported to induce a Th1 polarization, whereas cathepsin L inhibitor CLIK148 has been reported to induce a Th2 polarization. In this study, we pre-treated bone marrow-derived dendritic cells (BMDC) with CA074Me or CLIK148, followed by stimulation with a known pro-Th1 inducer (CpG) and a known pro-Th2 inducer (TNF-alpha) and analyzed by microarrays the expression of genes acting as pro-Th1 or pro-Th2 mediators.

2018-12-01 | GSE66738 | GEO

Impact of Acute methionine restriction on proteome of Th1 cells - Part 2

Project description:CD4 T cells were activated using CD3/CD28 antibodies in the presence of IL2 and IL12, to generate Th1 cells. Th1 cells were maintained and expanded in IL2 and IL12, on D5 Th1 cells were sorted for CD4+ expression and DAP1 exclusion. After flow sorting, live TH1 cells were resuspended (1e6 per ml) in methionine free RPMI, supplemented with 10% dialysed FBS, IL2 and IL12, and with L-methionine (100μM, or 1μM). Cells were cultured for 5 hrs before collection for proteomics processing.

2019-03-29 | PXD012053 | Pride

P2X7 signaling drives Th1 cell differentiation through metabolic reprogramming for aerobic glycolysis

Project description:This study provides evidence on the molecular mechanisms by which P2RX7 signaling promotes Th1 cell differentiation. P2RX7 induces T-bet expression and aerobic glycolysis in splenic CD4+ T cells that respond to malaria, at a time prior to Th1/Tfh polarization. Cell-intrinsic P2RX7 signaling sustains the glycolytic pathway and causes bioenergetic mitochondrial stress in activated CD4+ T cells. We also show in vitro the phenotypic similarities of Th1-polarized CD4+ T cells that do not express P2RX7 and those in which the glycolytic pathway is pharmacologically inhibited. In addition, ATP synthase blockade in vitro and the consequent inhibition of oxidative phosphorylation, which forces cells to use aerobic glycolysis, is sufficient to promote rapid CD4+ T cell proliferation and polarization to the Th1 profile in the absence of P2RX7. These data demonstrate that P2RX7-mediated metabolic reprograming for aerobic glycolysis is a key event for Th1 cell differentiation and suggest that ATP synthase inhibition is a fundamental mechanism by which P2X7 signaling induces the Th1 response.

2023-03-08 | PXD037754 | Pride

Pro-oxidant therapy by a vitamin K precursor targets PI 3-Kinase VPS34 function

Project description:Pro-oxidant therapy by a vitamin K precursor targets PI 3-Kinase VPS34 function

| PRJNA622809 | ENA

Vitamin C regulates Schwann cell myelination by promoting DNA demethylation of pro-myelinating genes

Project description:Vitamin C regulates Schwann cell myelination by promoting DNA demethylation of pro-myelinating genes

| PRJNA564620 | ENA

Maternal Vitamin D deficiency induces transcriptomic changes in newborn rat lungs

Project description:Transcriptomic analysis of lungs from newborn rats born to vitamin D adequate and vitamin D deficient mothers Vitamin D deficiency during pregnancy is common and is related to several maternal and fetal morbidities. Past studies suggest that vitamin D plays a role in normal lung development and we have shown that vitamin D regulates lung alveolar and vascular growth and preserves lung structure in experimental bronchopulmonary dysplasia (BPD) through improved pro-angiogeneic signaling. In addition, maternal vitamin D deficiency causes abnormal airway, alveolar, and vascular growth, as well as impaired lung function and airway hyper-reactivity in newborn rats. However, the mechanisms responsible for these physiologic effects are unknown. To gain insight into the role that maternal vitamin D status has on fetal lung development we used an unbiased transcriptomic approach to identify pathways altered in the lungs of offspring from vitamin D deficient dams.

2020-09-01 | GSE136736 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data