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ATAC-seq: Aryl hydrocarbon receptor governs a transcriptional programme that determines regulatory B cell differentiation and function

ABSTRACT: ATAC-seq: Aryl hydrocarbon receptor governs a transcriptional programme that determines regulatory B cell differentiation and function

PROVIDER: PRJEB30513 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3016190.fastq.gz	Fastqsanger.gz
	ERR3016200.fastq.gz	Fastqsanger.gz
	ERR3016191.fastq.gz	Fastqsanger.gz
	ERR3016201.fastq.gz	Fastqsanger.gz
	ERR3016182.fastq.gz	Fastqsanger.gz

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RNASeq: Aryl hydrocarbon receptor governs a transcriptional programme that determines regulatory B cell differentiation and function

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Project description:Regulatory B cells (Breg) play a critical role in the control of autoimmunity and inflammation. Although IL-10 is considered the hallmark for the identification of Bregs, the molecular programme that controls IL-10 production in Bregs is yet to be defined. Here, we demonstrate that aryl hydrocarbon receptor (AhR) controls the differentiation and function of IL-10-producing Bregs. Deficiency of AhR-expressing B cells drastically reduces IL-10 production by B cells. This leads to the unrestrained differentiation of T helper (Th)17 cells and a significant reduction in the percentage of regulatory T cells (Treg), which increases the severity of experimental arthritis when compared to control animals with AhR-sufficient B cells. A combination of chromatin-landscape profiling by ATAC-seq and transcriptome analyses by RNA-seq demonstrated that a loss of AhR expression in B cells not only reduces IL-10 expression by Bregs, defined as CD21hiCD24hi B cells, but also promotes a pro-inflammatory programme in CD21hiCD24hi B cells, even under Breg inducing conditions. Thus, AhR acts as a master transcriptional regulator of Breg differentiation by implementing a molecular programme that controls IL-10 production and represses pro-inflammatory cytokine production.

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