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Single-cell transcriptome analysis of CD3+ T lymphocytes from prurigo nodularis lesional skin reveals Th17 polarization

ABSTRACT: Single-cell transcriptome analysis of CD3+ T lymphocytes from prurigo nodularis lesional skin reveals Th17 polarization

PROVIDER: PRJNA882770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21657600_1.fastq.gz	Fastqsanger.gz
	SRR21657600_2.fastq.gz	Fastqsanger.gz
	SRR21657601_1.fastq.gz	Fastqsanger.gz
	SRR21657601_2.fastq.gz	Fastqsanger.gz
	SRR21657602_1.fastq.gz	Fastqsanger.gz

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Single-cell transcriptome analysis of CD3+ T lymphocytes from prurigo nodularis lesional skin reveals Th17 polarization

Project description:Prurigo nodularis (PN) is a chronic inflammatory skin disease characterized by symmetrically distributed, intensely pruritic nodules of unknown etiology and unmet therapeutic need. The lack of approved therapies and the limited efficacy of off-label treatments reflect the current poor understanding of its pathogenesis. We aimed to comprehensively characterize the phenotypic variation of CD3+ T cells and asses cell-specific gene expression in the lesional skin of patients with PN versus in patients with atopic dermatitis (AD) and in healthy controls (HC). To this end, single-cell RNA sequencing (scRNA-Seq) using 10x Genomics was carried out to compare CD3+ T cells transcriptomic heterogeneity between lesional samples of PN (n=6), AD (n=5) and HC (n=5).

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Project description:Prurigo nodularis (PN) is an intensely pruritic, inflammatory skin disease with a poorly understood pathogenesis. Thus, we performed single-cell transcriptomic profiling of 28,695 lesional and non-lesional PN cells. Lesional PN has increased dysregulated fibroblasts (FBs) and myofibroblasts. FBs in lesional PN were shifted towards a cancer-associated fibroblast (CAF)-like phenotype, with POSTN+WNT5A+ CAFs increased in PN, and similarly so in squamous cell carcinoma. A multi-center cohort study revealed an increased risk of SCC and CAF-associated malignancies (breast and colorectal) in PN patients. Systemic fibroproliferative diseases (renal sclerosis and idiopathic pulmonary fibrosis) were upregulated in PN patients. Ligand receptor analyses demonstrated a fibroblast neuronal axis with FB-derived WNT5A and periostin interactions with neuronal receptors MCAM and ITGAV. Compared to atopic dermatitis and psoriasis, mesenchymal dysregulation is unique to PN with an intermediate Th2/Th17 phenotype. These findings identify a pathogenic and targetable POSTN+WNT5A+ fibroblast subpopulation that may predispose CAF-associated malignancies in PN patients.

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