Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

C-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

ABSTRACT: c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

PROVIDER: PRJNA601925 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10908100_1.fastq.gz	Fastqsanger.gz
	SRR10908100_2.fastq.gz	Fastqsanger.gz
	SRR10908101_1.fastq.gz	Fastqsanger.gz
	SRR10908101_2.fastq.gz	Fastqsanger.gz
	SRR10908102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells.

Project description:RORγt+ group 3 innate lymphoid cells (ILC3s) maintain intestinal homeostasis through secretion of type 3 cytokines such as interleukin (IL)-17 and IL-22. However, CCR6- ILC3s additionally co-express T-bet allowing for the acquisition of type 1 effector functions. While T-bet controls the type 1 programming of ILC3s, the molecular mechanisms governing T-bet are undefined. Here, we identify c-Maf as a crucial negative regulator of murine T-bet+ CCR6- ILC3s. Phenotypic and transcriptomic profiling of c-Maf-deficient CCR6- ILC3s revealed a hyper type 1 differentiation status, characterized by overexpression of ILC1/NK cell-related genes and downregulation of type 3 signature genes. On the molecular level, c-Maf directly restrained T-bet expression. Conversely, c-Maf expression was dependent on T-bet and regulated by IL-1β, IL-18 and Notch signals. Thus, we define c-Maf as a crucial cell-intrinsic brake in the type 1 effector acquisition which forms a negative feedback loop with T-bet to preserve the identity of CCR6- ILC3s.

| S-EPMC7025824 | biostudies-literature

c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

Project description:We performed RNA-Seq analysis of small intestinal lamina propria ILC3s of Rorc.Cre Maf.flox and Maf.flox control mice.

2020-02-11 | GSE143867 | GEO

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [RNA-seq]

Project description:The transcription factor c-Maf is an essential regulator of group 3 ILC homeostasis and effector plasticity. c-Maf limits acquisition of the type 1 program and conversion to the ILC1 fate through restraint of T-bet expression and function.

2019-09-13 | GSE137321 | GEO

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [CUT&RUN]

2019-09-13 | GSE137320 | GEO

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [ATAC-seq]

2019-09-13 | GSE137319 | GEO

miRNA expression profile in CCR6+ regulatory T cells

Project description:To detect the miRNA expression profile in CCR6+ regulatory T cells In this study, the total RNA was extracted from CCR6+ regulatory T cells and CCR6- regulatory T cells. Then, the expression profile of miRNA on these cells was detected by microarray.

2014-08-05 | E-GEOD-60041 | biostudies-arrayexpress

WT vs c-Maf KO fetal liver macrophage

Project description:Homozygous disruption of c-Maf led to embryonic lethality and impaired erythroblastic island formation. c-Maf is expressed in the fetal liver macrophages. It suggests that macrophages are responsible for the lethality of c-Maf knock-out embryos. To search downstream genes of c-Maf, we surveyed genes associated with macrophage function by microarray analysis. keywords: c-Maf, macrophage, erythroblastic islands, WT (c-Maf WT) and c-Maf KO (c-Maf KO) fetal liver macrophages were sorted by a FACSAria cell sorter. Total RNAs from those macrophages were prepared using RNeasy Kit. Genes down-regulated in c-Maf KO macrophages were searched by GeneSpring software.

2011-07-06 | E-GEOD-23305 | biostudies-arrayexpress

Microarray data of REV-ERBa-deficient CCR6+ ILC3

Project description:Microarray was used to determine transcriptional differences between Nr1d1+/+ CCR6+ ILC3s and Nr1d1-/- CCR6+ ILC3s isolated from small intestine lamina propria

2019-08-29 | GSE136557 | GEO

Molecular mechanisms of HIV-1 permissiveness in CCR4+CCR6+ Th17 cells

Project description:We previously reported that CCR4+CCR6+Th17 cells are permissive to HIV, while CXCR3+CCR6- Th1 cells are relatively resistant. To identify molecular mechanisms underlying these differences, we performed a genome-wide transcriptional profiling in CXCR3+CCR6-Th1, CCR4+CCR6-Th2, CCR4+CCR6+Th17, and CXCR3+CCR6+Th1Th17 upon TCR triggering. Transcriptional differences between Th17 and Th1 were the most remarkable. HIV-DNA integration was highly efficient in Th17 versus Th1 upon exposure to both wild-type and VSV-G-pseudotyped HIV, indicative that post-entry mechanisms contribute to HIV permissiveness. 4 cell populations from up to 5 donors for a total of 19 samples.

2015-08-30 | E-GEOD-70396 | biostudies-arrayexpress

Molecular mechanisms of HIV-1 permissiveness in CCR4+CCR6+ Th17 cells

2015-08-30 | GSE70396 | GEO