A novel approach for studying mast cell-driven disorders: mast cells derived from induced pluripotent stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA752100 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15343236_1.fastq.gz | Fastqsanger.gz | |||
| SRR15343236_2.fastq.gz | Fastqsanger.gz | |||
| SRR15343237_1.fastq.gz | Fastqsanger.gz | |||
| SRR15343237_2.fastq.gz | Fastqsanger.gz | |||
| SRR15343238_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
Similar Datasets
Project description:We developed a novel strategy for the rapid and efficient differentiation of MCs from human induced pluripotent stem cells (hiPSC). These hiPSC-derived MCs (hiPSC-MCs) exhibit phenotypic and functional characteristics of human skin MCs (hsMCs) and peripheral hematopoietic stem cell-derived MCs (PSCMCs). hiPSC-MCs display stable expression of MC-associated receptors such as CD117, FcεRIα and MRGPRX2, and degranulate by stimulation with IgE/anti-IgE and Substance. P.
2022-08-31 | GSE181457 | GEO
Project description:Intestinal mucosal mast cells are critically involved in the development of food-induced allergic disorders. However, factors that induce differentiation of mucosal mast cells in the intestinal mucosa are largely unknown. To identify factors involved in mucosal mast cell differentiation, we compared the gene expression profiles between mucosal mast cells isolated from the small intestine and bone marrow-derived mast cells cultured in the presence of TGF-β or Notch ligand.
2016-06-15 | GSE80139 | GEO
Project description:Intestinal mucosal mast cells are critically involved in the development of food-induced allergic disorders. However, factors that induce differentiation of mucosal mast cells in the intestinal mucosa are largely unknown. To identify factors involved in mucosal mast cell differentiation, we compared the gene expression profiles between mucosal mast cells isolated from the small intestine and bone marrow-derived mast cells cultured in the presence of TGF-β or Notch ligand. Mucosal mast cells were isolated from the small intestine of naïve BALB/c mice by flow cytometry. Bone marrow-derived mast cells (BMMCs) were generated by culturing BALB/c bone marrow cells with murine interleukin-3 and stem cell factor for 3-4 weeks, and then cells were cultured for 6 days in the presence or absence of TGF-β or Delta-like 1 (Dll1), which is a Notch ligand. Total RNAs extracted from these cells were processed and hybridized to Affymetrix GeneChips.
2016-06-15 | E-GEOD-80139 | biostudies-arrayexpress
Project description:Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mouse bone marrow-derived mast cells were treated with IL3, IL3+IL33, or IL3+SCF. Six replicates each.
2012-05-01 | E-GEOD-35332 | biostudies-arrayexpress
Project description:The difference between intraepithelial mast cells and lamina propria mast cells
| PRJNA981202 | ENA
Project description:Type 2 immune responses are crucial for protection against helminth infections and for the maintenance of tissue homeostasis, yet the underlying mechanisms of immune activation remain incompletely understood. Here, we study the role of mast cells in type 2 immunity. While the number of lamina propria residing mast cells (termed LPMCs hereinafter) remained stable, intraepithelial mast cells (termed IEMCs hereinafter) markedly expanded during the course of type 2 responses. We uncovered a new type 2 response mechanism depending on the crosstalk between mast cells and epithelial cells, and defined the function of intraepithelial mast cells.
2024-04-15 | GSE234414 | GEO
Project description:Mast cells are known to be the key players in type I hypersensitivity reactions in humans and mice. They are critically involved in the development of allergic rhinitis, allergic asthma and systemic anaphylaxis. In this study we investigated the role of the transcriptional regulator MAZR in mast cells by comparing the expression profile of mast cells generated from wild-type (MazrF/F) and MAZR-deficient (MazrF/F x Vav-iCre) bone marrow cells. Our results from the array data demonstrate that MAZR acts preferentially as a transcriptional repressor in mast cells.
2013-10-18 | E-MTAB-1816 | biostudies-arrayexpress
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. Mast cell maturation; immature and mature bone marrow-derived mast cells (BMMCs); Four-condition experiment (mature BMMCs vs immature BMMCs, Pla2g3M-bM-^@M-^S/M-bM-^@M-^S vs Pla2g3+/+); 3 replicates of Pla2g3+/+ BMMCs, 4 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S BMMCs, 4 replicates of Pla2g3+/+ cocultured BMMCs, 3 replicates of Pla2g3M-bM-^@M-^S/M-bM-^@M-^S cocultured BMMCs
2013-03-09 | E-GEOD-44980 | biostudies-arrayexpress
Project description:Type 2 immune responses are crucial for protection against helminth infections and for the maintenance of tissue homeostasis, yet the underlying mechanisms of immune activation remain incompletely understood. Here, we study the role of mast cells in type 2 immunity. While the number of lamina propria residing mast cells (termed LPMCs hereinafter) remained stable, intraepithelial mast cells (termed IEMCs hereinafter) markedly expanded during the course of type 2 responses. We uncovered a new type 2 response mechanism depending on the crosstalk between mast cells and epithelial cells, and defined the function of intraepithelial mast cells.
2024-04-15 | GSE252202 | GEO
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