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

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

PROVIDER: PRJNA565167 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10103443_1.fastq.gz	Fastqsanger.gz
	SRR10103443_2.fastq.gz	Fastqsanger.gz
	SRR10103444_1.fastq.gz	Fastqsanger.gz
	SRR10103444_2.fastq.gz	Fastqsanger.gz
	SRR10103445_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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 | GSE137320 | GEO

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

Project description:c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program

| PRJNA565163 | ENA

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

2019-09-13 | GSE137321 | 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

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

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

| PRJNA565166 | ENA

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

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

| PRJNA565165 | ENA

c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program.

Project description:CCR6- group 3 innate lymphoid cells (ILC3s) are mediators of intestinal immunity and barrier function that possess the capacity to acquire type 1 effector features and fully convert into ILC1s. The molecular mechanisms governing such plasticity are undefined. Here, we identified c-Maf as an essential regulator of ILC3 homeostasis and plasticity that limits physiological ILC1 conversion. Phenotypic analysis of effector status in Maf-deficient CCR6- ILC3s, coupled with evaluation of global changes in transcriptome, chromatin accessibility, and transcription factor motif enrichment, revealed that c-Maf enforces ILC3 identity. c-Maf promoted ILC3 accessibility and supported ROR?t activity and expression of type 3 effector genes. Conversely, c-Maf antagonized type 1 programming, largely through restraint of T-bet expression and function. Mapping of the dynamic changes in chromatin landscape accompanying CCR6- ILC3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type 1 regulatory transformation and a controller of ILC3 fate.

| S-EPMC7037249 | biostudies-literature

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-09-13 | GSE137322 | GEO

Study of the role of c-Maf in type 2 innate lymphoid cells

Project description:Group 2 innate lymphoid cells (ILC2s) are involved in type 2 inflammatory diseases such as allergy. In response to repeated allergen inhalations, lung epithelial cells secrete innate cytokines that activate ILC2s to release interleukin-5 (IL-5) and interleukin-13 (IL-13) resulting in eosinophil infiltration, mucus hyper-production, and airway hyperreactivity. Beside GATA3, very little is known about the role of specific transcription factors in the regulation of ILC2’s function. Here we identify c-Maf as a crucial regulator of ILC2 function and identity. c-Maf deficient ILC2s are impaired in IL-5 and IL-13 production and eosinophil recruitment. Transcriptomic analysis underlined a reduced expression of genes associated with Th2/ILC2 identity and memory development that we confirmed both in mice and human, either in ILC2s engineered to express less c-Maf or in naturally c-Maflow ILC2s from cord blood. Our results indicate that c-Maf is a core node that connects immature to primed/trained ILC2s.

2022-04-20 | GSE166739 | GEO

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

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