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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Notch signaling promotes differentiation of mouse mucosal mast cells

ABSTRACT: 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-Î² or Notch ligand. Mucosal mast cells were isolated from the small intestine of naÃ¯ve 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-Î² or Delta-like 1 (Dll1), which is a Notch ligand. Total RNAs extracted from these cells were processed and hybridized to Affymetrix GeneChips.

ORGANISM(S): Mus musculus

SUBMITTER: Nobuhiro Nakano

PROVIDER: E-GEOD-80139 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Notch signaling promotes differentiation of mouse mucosal mast cells

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

MicroRNA profiling of mouse bone marrow-derived mast cells during mucosal differentiation and IgE-mediated activation

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Stem cell factor programs the mast cell activation phenotype

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.

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Induction of Interleukin-9-producing Mucosal Mast cells Promotes Susceptibility to IgE-mediated Experimental Food Allergy

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SCF -licensed induction of a mucosal mast cell-like transcriptional program by TGF-b

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2020-08-03 | GSE155571 | GEO

Two functionally distinct subsets of mast cells generated through IL-2 independent CD25 activities

Project description:CD25 (IL-2R) can be expressed on the surface of immune cells in the absence of other chains of the interleukin-2 receptor (IL-2R), which are indispensable for IL-2 signaling. We identified two novel mast cell subsets, characterized by the differential expression of surface CD25, and by the ability to produce different cytokines and to proliferate, both in vitro and in vivo. We provide evidence that functional differences between the two mast cell populations were dependent on CD25 itself, which directly modulated mast cell proliferation and responses in vivo. These effects were completely independent from IL-2 or the expression of the other chains of the high-affinity IL-2R, indicating an autonomous and previously unappreciated role for CD25 in regulating cell functions. Similar results were also obtained in dendritic cells, which are known to express CD25 but to be unresponsive to IL-2. Our findings indicate a general role for CD25 in contexts where IL-2 signaling is not involved, and may have important implications for all mast cell-related diseases, including mastocytosis, where CD25 is aberrantly expressed on pathogenic mast cells. Total mRNA of FACS-sorted CD25pos and CD25neg populations of primary bone marrow-derived mast cells (BMMCs) was extracted and subjected to by multiparallel sequencing.

2014-08-03 | E-GEOD-52502 | biostudies-arrayexpress

Gene expression profiling of BMMC derived-MMCs and BMMC-derived CTMCs.

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2022-07-28 | GSE135148 | GEO

Mast Cell Maturation is Driven via a Novel Group III Phospholipase A2-Prostaglandin D2-DP1 Receptor Paracrine Axis

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2013-03-09 | E-GEOD-44980 | biostudies-arrayexpress

Mast cell expression data from murine aryl hydrocarbon receptor (AhR) null, AhR_d and normal control mice

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