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Single-cell transcriptomic analysis of dermal macrophage from PDGFRa-lineage origin under atopic dermatitis

ABSTRACT: Single-cell transcriptomic analysis of dermal macrophage from PDGFRa-lineage origin under atopic dermatitis

PROVIDER: PRJNA702126 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13721828_1.fastq.gz	Fastqsanger.gz
	SRR13721828_2.fastq.gz	Fastqsanger.gz
	SRR13721829_1.fastq.gz	Fastqsanger.gz
	SRR13721829_2.fastq.gz	Fastqsanger.gz
	SRR13721830_1.fastq.gz	Fastqsanger.gz

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Single-cell transcriptomic analysis of dermal macrophage from PDGFRa-lineage origin under atopic dermatitis

Project description:We analyzed dermal macrophage repertoire derived from PDGFRa-lineage or non-PDGFRa-lineage origin in atopic dermatitis (AD) with single-cell RNA sequencing. PDGFRa-lineage tracing mice aged between 7- and 14-week old were used to label cells of PDGFRa-lineage with tdTomato. AD was induced by topic application of MC903 bidaily or tridaily to skin of female mice for six times. Inflamed skin was excised on day 14 and single cells were prepared. Target cells were sorted as single cells for sequencing. We identified multiple subtypes in both PDGFRa-lineage or non-PDGFRa-lineage macrophage and the proportion differed by PDGFRa-lineage origin in AD skin.

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Project description:Atopic dermatitis and psoriasis are driven by alternate type 2 and type 17 immune responses, but some proteins might be critical to both diseases. We show that a deficiency of the TNF superfamily molecule TWEAK (TNFSF12) in mice results in defective maintenance of atopic dermatitis-specific Th2 and psoriasis-specific Th17 cells in the skin, and impaired expression of disease-characteristic chemokines and cytokines, such as CCL17 and TSLP in atopic dermatitis, and CCL20 and IL-19 in psoriasis. The TWEAK receptor, Fn14, is upregulated in keratinocytes and dermal fibroblasts, and TWEAK induces these cytokines and chemokines alone and in synergy with the signature T helper cytokines of either disease, IL-13 and IL-17. Furthermore, subcutaneous injection of recombinant TWEAK into naïve mice induces cutaneous inflammation with histological and molecular signs of both diseases. TWEAK is therefore a critical contributor to skin inflammation and a possible therapeutic target in atopic dermatitis and psoriasis.

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Project description:Atopic dermatitis is increasing worldwide, correlating with air pollutions. Various organic components of pollutants activate transcription factor AhR (aryl-hydrocarbon receptor). We have established AhR-CA mice, whose keratinocytes express constitutive-active AhR, and these mice developed atopic dermatitis-like frequent scratching and allergic inflammation. In this study we performed ChIP-seq analyses and identified keratinocyte-specific AhR target genes, including inflammatory cytokines Tslp and IL33, and neurotrophic factor Artemin. While AhR-CA mice exhibited epidermal hyperinnervation and alloknesis leading to hypersensitivity to pruritus, blockade of Artemin alleviated these phenotypes. AhR-CA mice showed scratching-induced barrier insufficiency and enhanced sensitization to epicutaneously-applied antigens, recapitulating human atopic dermatitis. Consistently, AhR activation and Artemin expression was detected in the epidermis of atopic dermatitis patients and keratinocytes exposed to air pollutants. Thus, AhR in keratinocytes senses the environmental stimuli and responds to them through moderating inflammation. We propose a mechanism in which air pollution induces atopic dermatitis through AhR activation.

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