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Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses

ABSTRACT: Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses

PROVIDER: PRJNA506378 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8225280_1.fastq.gz	Fastqsanger.gz
	SRR8225280_2.fastq.gz	Fastqsanger.gz
	SRR8225275_1.fastq.gz	Fastqsanger.gz
	SRR8225275_2.fastq.gz	Fastqsanger.gz
	SRR8225276_1.fastq.gz	Fastqsanger.gz

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Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses

Project description:To identify the molecular mechanisms responsible for enhanced atopic dermatitis (AD) pathogenesis upon Ets1 deficiency in CD4+ T cells, we compared transcriptome profile between CD4+ T cells from littermate control (LMC) and Ets1ΔdLck mice at the peak of AD progression by performing RNA-seq.

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Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses.

Project description:Atopic dermatitis (AD) is a complex inflammatory skin disease mediated by immune cells of both adaptive and innate types. Among them, CD4+ Th cells are one of major players of AD pathogenesis. Although the pathogenic role of Th2 cells has been well characterized, Th17/Th22 cells are also implicated in the pathogenesis of AD. However, the molecular mechanisms underlying pathogenic immune responses in AD remain unclear. We sought to investigate how the defect in the AD susceptibility gene, Ets1, is involved in AD pathogenesis in human and mice and its clinical relevance in disease severity by identifying Ets1 target genes and binding partners. Consistent with the decrease in ETS1 levels in severe AD patients and the experimental AD-like skin inflammation model, T cell-specific Ets1-deficient mice (Ets1ΔdLck) developed severe AD-like symptoms with increased pathogenic Th cell responses. A T cell-intrinsic increase of gp130 expression upon Ets1 deficiency promotes the gp130-mediated IL-6 signaling pathway, thereby leading to the development of severe AD-like symptoms. Functional blocking of gp130 by selective inhibitor SC144 ameliorated the disease pathogenesis by reducing pathogenic Th cell responses. Our results reveal a protective role of Ets1 in restricting pathogenic Th cell responses and suggest a potential therapeutic target for AD treatment.

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