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ChIP-seq analysis of ETV3 and ETV6 in monocyte-derived cells

ABSTRACT: ChIP-seq analysis of ETV3 and ETV6 in monocyte-derived cells

PROVIDER: PRJNA871109 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21136800_1.fastq.gz	Fastqsanger.gz
	SRR21136800_2.fastq.gz	Fastqsanger.gz
	SRR21136801_1.fastq.gz	Fastqsanger.gz
	SRR21136801_2.fastq.gz	Fastqsanger.gz
	SRR21136802_1.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis of ETV3 and ETV6 in monocyte-derived cells

Project description:We analyzed by ChIPseq the genes bound by ETV3 or ETV6 in differentiating monocytes.

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RNA-seq analysis of human monocytes exposed to lentivirus expressing shRNA against ETV3 or ETV6 during differentiation

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Transcription factor Etv3 controls the tolerogenic function of dendritic cells (RNA-seq of Etv3 KO Tregs)

Project description:Dendritic cells (DC) facilitate the maintenance of immunological tolerance in the steady state. We report that transcription factor Etv3 is preferentially expressed in mature DC including tissue-derived migratory DC (migDC), and facilitates their homeostatic maturation and CCR7-dependent migration. Mice with global or DC-specific deletion of Etv3 manifested the expansion of CD25low regulatory T cells (Treg), spontaneous activation of conventional T cells, and multiorgan T cell infiltration. Etv3 deficiency exacerbated TLR7-driven systemic lupus erythematosus (SLE)-like disease, supporting the reported genetic association of human ETV3 with SLE. Etv3-deficient migDC upregulated multiple costimulatory molecules including OX40 ligand (OX40L/TNFSF4), whose blockade partially rescued the Treg abnormalities. These results identify Etv3 as an essential regulator of the tolerogenic function of DC, and implicate it in the regulation of human autoimmunity.

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Transcription factor Etv3 controls the tolerogenic function of dendritic cells (RNA-seq of Etv3 KO GM-DCs)

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ETV3 and ETV6 enable monocyte differentiation into dendritic cells by repressing macrophage fate commitment.

Project description:In inflamed tissues, monocytes differentiate into macrophages (mo-Macs) or dendritic cells (mo-DCs). In chronic nonresolving inflammation, mo-DCs are major drivers of pathogenic events. Manipulating monocyte differentiation would therefore be an attractive therapeutic strategy. However, how the balance of mo-DC versus mo-Mac fate commitment is regulated is not clear. In the present study, we show that the transcriptional repressors ETV3 and ETV6 control human monocyte differentiation into mo-DCs. ETV3 and ETV6 inhibit interferon (IFN)-stimulated genes; however, their action on monocyte differentiation is independent of IFN signaling. Instead, we find that ETV3 and ETV6 directly repress mo-Mac development by controlling MAFB expression. Mice deficient for Etv6 in monocytes have spontaneous expression of IFN-stimulated genes, confirming that Etv6 regulates IFN responses in vivo. Furthermore, these mice have impaired mo-DC differentiation during inflammation and reduced pathology in an experimental autoimmune encephalomyelitis model. These findings provide information about the molecular control of monocyte fate decision and identify ETV6 as a therapeutic target to redirect monocyte differentiation in inflammatory disorders.

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Monocyte-derived Macrophages

Project description:Monocyte-derived Macrophages

| PRJNA948022 | ENA