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Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [triplicates]

ABSTRACT: Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [triplicates]

PROVIDER: PRJNA925184 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23111219.fastq.gz	Fastqsanger.gz
	SRR23111220.fastq.gz	Fastqsanger.gz
	SRR23111221.fastq.gz	Fastqsanger.gz
	SRR23111222.fastq.gz	Fastqsanger.gz
	SRR23111223.fastq.gz	Fastqsanger.gz

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Similar Datasets

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [triplicates]

Project description:To investigate the cooperative function of dermal fibroblast and mast cell in inducing mast cell tolerance to commensals We then performed gene expression profiling analysis using data obtained from RNA-seq of mast cells, and mast cells conditioned by dermal fibroblasts before and after treatments with commensal bacteria supernatants.

2023-05-02 | GSE223179 | GEO

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [LTA]

2023-05-02 | GSE223177 | GEO

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts

Project description:Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts

| PRJNA925177 | ENA

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [LTA]

Project description:Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [LTA]

| PRJNA925178 | ENA

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [single-cell RNA-seq]

Project description:Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [single-cell RNA-seq]

| PRJNA925179 | ENA

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts [single-cell RNA-seq]

Project description:To investigate the cooperative function of dermal fibroblast and mast cell in inducing mast cell tolerance to commensals We then performed gene expression profiling analysis using data obtained from SC RNA seq of mast cells, dermal fibroblast and and mast cells in co culture with dermal fibroblasts .

2023-05-02 | GSE223178 | GEO

Synovial microenvironment-influenced mast cells promote the progression of rheumatoid arthritis

Project description:Mast cells are phenotypically and functionally highly heterogeneous, and their state is possibly controlled by their local microenvironment. Therefore, concrete analyses are needed to understand whether mast cells act as powerful motivators or dispensable bystanders in specific diseases. Here, we evaluated the correlation between synovial mast cells and rheumatoid arthritis (RA) disease severity, and the efficacy of therapeutic interventions against mast cells. We showed that degranulation of mast cells in inflammatory synovial tissues of RA patients was induced via MAS-related G protein-coupled receptor X2 (MRGPRX2), and the expression of MHC class II (MHC II) and costimulatory molecules on mast cells were upregulated. These unique signaling response led to mast cell activation and promoted T cell responses, resulting in the progression of RA. Collagen-induced arthritis mouse models treated with a combination of anti-IL-17A and cromolyn sodium, a mast cell membrane stabilizer, showed significantly reduced clinical severity and decreased bone erosion. The findings of the present study suggest that synovial microenvironment-influenced mast cells contribute to RA and may provide a novel mast cell-targeting therapy for RA.

2024-01-07 | PXD038584 | Pride

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts.

Project description:Activation and degranulation of mast cells (MCs) is an essential aspect of innate and adaptive immunity. Skin MCs, the most exposed to the external environment, are at risk of quickly degranulating with potentially severe consequences. Here, we define how MCs assume a tolerant phenotype via crosstalk with dermal fibroblasts (dFBs) and how this phenotype reduces unnecessary inflammation when in contact with beneficial commensal bacteria. We explore the interaction of human MCs (HMCs) and dFBs in the human skin microenvironment and test how this interaction controls MC inflammatory response by inhibiting the nuclear factor κB (NF-κB) pathway. We show that the extracellular matrix hyaluronic acid, as the activator of the regulatory zinc finger (de)ubiquitinating enzyme A20/tumor necrosis factor α-induced protein 3 (TNFAIP3), is responsible for the reduced HMC response to commensal bacteria. The role of hyaluronic acid as an anti-inflammatory ligand on MCs opens new avenues for the potential treatment of inflammatory and allergic disorders.

| S-EPMC10290424 | biostudies-literature

Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts

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

2023-05-02 | GSE223180 | GEO

Effects of group III phospholipase A2 deficiency in mast cells on fibroblast-directed maturation of mast cells in vitro

Project description:Microenvironment-based alterations in mast cell phenotypes influence the susceptibility to anaphylaxis, yet the mechanisms underlying proper maturation of mast cells toward an anaphylaxis-sensitive phenotype are incompletely understood. Here we report that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A2, regulates this process. PLA2G3 secreted from mast cells is coupled with fibroblastic lipocalin-type PGD2 synthase (L-PGDS) to provide PGD2, which facilitates mast cell maturation via PGD2 receptor (DP1). Mice lacking PLA2G3, L-PGDS or DP1, mast cell-deficient mice reconstituted with PLA2G3- or DP1-null mast cells, or mast cells cocultured with L-PGDS-ablated fibroblasts exhibited impaired mast cell maturation and anaphylaxis. Thus, we describe a lipid-driven PLA2G3-L-PGDS-DP1 loop that drives mast cell maturation.

2013-03-09 | GSE44980 | GEO

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