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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

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			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

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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.

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

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