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Regulation of the alveolar regenerative niche by amphiregulin-producing Treg cells

ABSTRACT: Regulation of the alveolar regenerative niche by amphiregulin-producing Treg cells

PROVIDER: PRJNA715236 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13995000.fastq.gz	Fastqsanger.gz
	SRR13995001.fastq.gz	Fastqsanger.gz
	SRR13995002_1.fastq.gz	Fastqsanger.gz
	SRR13995002_2.fastq.gz	Fastqsanger.gz
	SRR13995003_1.fastq.gz	Fastqsanger.gz

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

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Regulation of the alveolar regenerative niche by amphiregulin-producing Treg cells (10X)

Project description:This study investigates the role of regulatory T cell–derived Areg on lung regeneration following influenza infection. We use single-cell RNA sequencing to capture the heterogeneity of lung mesenchymal populations during influenza infection. Here, we probe the gene expression changes within stromal cells from wildtype mice and in mice that conditionally lack Areg from T cell sources (CD4-cre Areg-flox) at day 8 post infection with PR8/H1N1. n = 1 per genotype.

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Project description:This study investigates the role of regulatory T cell–derived Areg in driving epithelial repair following influenza infection. We use RNA sequencing to probe the gene expression changes within epithelial cells in wildtype mice and in mice that conditionally lack Areg from T cell sources (CD4-cre Areg-flox). Further, we identify a population of damage-associated transitional alveolar epithelial cells that are induced in reponse to acute injury and exhibit gene expression changes reflective of AT2 transdifferentiation to AT1.

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Regulation of the alveolar regenerative niche by amphiregulin-producing Treg cells (MesSTIM)

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Regulation of the alveolar regenerative niche by amphiregulin-producing regulatory T cells.

Project description:Following respiratory viral infection, regeneration of the epithelial barrier is required to preserve lung function and prevent secondary infections. Lung regulatory T (Treg) cells are critical for maintaining blood oxygenation following influenza virus infection through production of the EGFR ligand amphiregulin (Areg); however, how Treg cells engage with progenitors within the alveolar niche is unknown. Here, we describe local interactions between Treg cells and an Areg-responsive population of Col14a1+EGFR+ lung mesenchymal cells that mediate type II alveolar epithelial (AT2) cell-mediated regeneration following influenza virus infection. We propose a mechanism whereby Treg cells are deployed to sites of damage and provide pro-survival cues that support mesenchymal programming of the alveolar niche. In the absence of fibroblast EGFR signaling, we observe impaired AT2 proliferation and disrupted lung remodeling following viral clearance, uncovering a crucial immune/mesenchymal/epithelial network that guides alveolar regeneration.

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2022-12-14 | GSE169124 | GEO

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