Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

ABSTRACT: TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

PROVIDER: PRJNA814714 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18293100.fastq.gz	Fastqsanger.gz
	SRR18293101.fastq.gz	Fastqsanger.gz
	SRR18293102.fastq.gz	Fastqsanger.gz
	SRR18293103.fastq.gz	Fastqsanger.gz
	SRR18293089.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq03, bulk-RNAseq)

Project description:TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq03, bulk-RNAseq)

| PRJNA810195 | ENA

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq04, scRNA-seq)

Project description:TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq04, scRNA-seq)

| PRJNA812500 | ENA

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq01, bulk-RNAseq)

Project description:TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq01, bulk-RNAseq)

| PRJNA814700 | ENA

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq05, bulk-RNAseq)

Project description:TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq05, bulk-RNAseq)

| PRJNA1017491 | ENA

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq05, bulk-RNAseq)

Project description:We have shown that TGFb in combination with IL-6 potently induces a T follicular helper cell (Tfh) cell phenotype in activated murine CD4+ T cells in vitro. The transcription factor c-Maf critically contributes to the differentiation of Tfh cells in vitro and in vivo.

2024-03-01 | GSE243257 | GEO

TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf (Seq02, bulk-RNAseq)

Project description:Naive murine CD4+ T cells from GREAT/SMART-17A mice were cultured under Th1 or Tfh(1 ng/ml TGF-β)-polarizing conditions in 96-well plates coated with anti-CD3/anti-CD28 for 3.5 days; sorted by flow cytometry on IFNg+ (Th1), or CXCR5-IL17A+ (Th17) and CXCR5+IL17A- (Tfh); and subjected to bulk RNA-seq.

2024-03-01 | GSE198374 | GEO

Signatures of murine PP Th17 derived Tfh cells

Project description:To determine the clinical relevance of the murine Th17-derived Tfh signatures in RA patients, we generated both splenic and PP murine Th17-derived Tfh cells signatures using bulk RNA-seq data.

2025-02-24 | GSE259259 | GEO

Jarid2, a Polycomb member and target of miR-155, regulates the fates of Th17 and Treg cells

Project description:Genome-wide analysis of Jarid2, Suz12, and c-Maf binding and H3K27me3 profiling in miR-155 KO and WT Th17 performed by ChIP-seq. We found that Jarid2 and c-Maf is differentially expressed in absence of miR-155 and they compete for binding to the Il22 promoter. We highlight targets of Jarid2 and Suz12 in miR-155 KO Th17 cells that are epigenetically silenced by increased H3K27me3 status. Furthermore, genome-wide analysis through Suz12 ChIP-exo in WT and Jarid2fl/fl;CD4cre Th17 reveals defects in PRC2 recruitment in abscence of Jarid2 that results in derepression of genes in Th17 cells. Thus, one main function of miR-155 is to curb epigenetic silencing by targeting Jarid2. Examination of Jarid2, Suz12, c-Maf binding and H3K27me3 changes in miR-155 KO and WT Th17.

2014-06-01 | E-GEOD-47528 | biostudies-arrayexpress

ScRNA-seq trajectory analysis of Th17, Tfh17, and exTh17-Tfh cells

Project description:This experiment was designed to study the functional differences between the Th17-derived Tfh and regular Tfh cells. To achieve these goals, we performed flow sorting and enriched CD4+ T cells from Current-Ex Th17 fate-mapping mice. We then performed scRNA seq analysis to compare the transcriptomic profiles of Tfh cells.

2025-02-24 | GSE290034 | GEO

Germinal Center T follicular helper (GC-Tfh) cell impairment in chronic HIV infection involves c-Maf signaling [microarray]

Project description:We have recently demonstrated that the function of T follicular helper (Tfh) cells obtained from lymph nodes (LN) of HIV-infected individuals is impaired. We found that these cells were unable to provide proper help to germinal center (GC)-B cells, as observed by altered and inefficient anti-HIV antibody response and premature death of memory B cells. The underlying molecular mechanisms of this dysfunction remain poorly defined. Herein, we have used a unique transcriptional approach to identify these molecular defects. We consequently determined the transcriptional profiles of LN GC-Tfh cells following their interactions with LN GC-B cells from HIV-infected and HIV-uninfected individuals, rather than analyzing resting ex-vivo GC-Tfh cells. We observed that proliferating HIV-infected GC-Tfh cells were transcriptionally different than those from HIV-uninfected individuals, displaying a significant downregulation of immune- and GC-Tfh-associated pathways and genes compared to cells from uninfected individuals. Our results strongly demonstrated that MAF (coding for the transcription factor c-Maf) and its upstream signaling pathway mediators (IL6R and STAT3) were significantly downregulated in HIV-infected subjects, which could contribute to the impaired GC-Tfh and GC-B cell functions reported during infection. We further showed that c-Maf function was associated with the adenosine pathway and that the signaling upstream c-Maf could be partially restored by adenosine deaminase -1 (ADA-1) supplementation. Overall, we identified a novel mechanism that contributes to GC-Tfh impairment during HIV infection. Understanding how GC-Tfh function is altered in HIV is crucial and could provide critical information about the mechanisms leading to the development and maintenance of effective anti-HIV antibodies.

2021-07-19 | GSE175728 | 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