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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

ABSTRACT: IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

PROVIDER: PRJNA961680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24298917_1.fastq.gz	Fastqsanger.gz
	SRR24298917_2.fastq.gz	Fastqsanger.gz
	SRR24298918_1.fastq.gz	Fastqsanger.gz
	SRR24298918_2.fastq.gz	Fastqsanger.gz
	SRR24298919_1.fastq.gz	Fastqsanger.gz

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

Project description:The complex system by which the skin regulates immune responses to the external environment is unclear. Here, we investigated cell-cell interactions underlying cutaneous defense against S. aureus. Single-cell transcriptomics (scRNA-Seq) and unbiased network analysis revealed unexpected, dominant IL-17-mediated dermal reticular fibroblast-to-neutrophil communication. Multi-faceted in vitro omics studies demonstrated that IL-17 synergized with several factors including TNF⍺ to induce fibroblast NFKBIZ and chemokine secretion. Cultured fibroblasts drove robust neutrophil recruitment through NFKBIZ-dependent CXCR2 and CXCR4 ligands. Mice lacking IL-17R in fibroblasts (PdgfraΔIl17ra) were generated to determine the significance of fibroblast-neutrophil communication. PdgfraΔIl17ra mice exhibited drastically reduced skin neutrophilia in multiple disease models and reduced defense against S. aureus. These findings were translated to humans by comprehensive analysis of biopsies from psoriasis patients on and off anti-IL-17 treatment. Thus, dermal fibroblasts are critical for skin type 17 inflammation and represent a novel target for treatment of infection and inflammatory disease.

2024-02-15 | GSE230512 | GEO

IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

2024-02-14 | GSE230511 | GEO

IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

Project description:IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

| PRJNA961668 | ENA

IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

Project description:IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

| PRJNA961678 | ENA

scRNAseq of aging dermal fibroblasts

Project description:scRNAseq of aging dermal fibroblasts

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-02-14 | GSE230513 | GEO

Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet's syndrome [Nanostring CosMx SMI spatial transcriptomics]

Project description:Sweet’s syndrome is a poorly understood inflammatory skin disease characterized by neutrophil infiltration to the dermis. Single-nucleus and bulk transcriptomics of archival clinical samples of Sweet’s syndrome revealed a prominent interferon signature in Sweet’s syndrome skin that was reduced in tissue from another neutrophilic dermatosis, pyoderma gangrenosum, as well as healthy controls. This signature was observed in different subsets of cells, including fibroblasts that expressed interferon-induced genes. Functionally, this response was supported by analysis of cultured primary human dermal fibroblasts that were observed to highly express neutrophil chemokines in response to activation by type I interferon. Furthermore, single-molecule resolution spatial transcriptomics of skin in Sweet’s syndrome identified positionally distinct immune-acting fibroblasts that included a CXCL1+ subset proximal to neutrophils and a CXCL12+ subset distal to the neutrophilic infiltrate. This study defines the cellular landscape of neutrophilic dermatoses and suggests dermal immune-acting fibroblasts play a role in the pathogenesis of Sweet’s syndrome through recognition of type I interferons.

2025-08-22 | GSE297091 | GEO

Regulation of Dermal Fibroblasts by Human Neutrophil Peptides

Project description:Regulation of Dermal Fibroblasts by Human Neutrophil Peptides

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CXCL12+ dermal fibroblasts promote neutrophil recruitment and host defense by recognition of IL-17.

Project description:The skin provides an essential barrier for host defense through rapid action of multiple resident and recruited cell types, but the complex communication network governing these processes is incompletely understood. To define these cell-cell interactions more clearly, we performed an unbiased network analysis of mouse skin during invasive S. aureus infection and revealed a dominant role for CXCL12+ fibroblast subsets in neutrophil communication. These subsets predominantly reside in the reticular dermis, express adipocyte lineage markers, detect IL-17 and TNFα, and promote robust neutrophil recruitment through NFKBIZ-dependent release of CXCR2 ligands and CXCL12. Targeted deletion of Il17ra in mouse fibroblasts resulted in greatly reduced neutrophil recruitment and increased infection by S. aureus. Analogous human CXCL12+ fibroblast subsets abundantly express neutrophil chemotactic factors in psoriatic skin that are subsequently decreased upon therapeutic targeting of IL-17. These findings show that CXCL12+ dermal immune acting fibroblast subsets play a critical role in cutaneous neutrophil recruitment and host defense.

| S-EPMC10890925 | biostudies-literature

Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet's syndrome.

Project description:Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet's syndrome.

| PRJNA1273167 | ENA

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