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

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

PROVIDER: PRJNA565163 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10103425_1.fastq.gz	Fastqsanger.gz
	SRR10103425_2.fastq.gz	Fastqsanger.gz
	SRR10103426_1.fastq.gz	Fastqsanger.gz
	SRR10103426_2.fastq.gz	Fastqsanger.gz
	SRR10103427_1.fastq.gz	Fastqsanger.gz

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

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

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

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

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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]

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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.

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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.

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

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