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Genome-wide analyses of chromatin state in human mast cells reveal molecular drivers and mediators of allergic and inflammatory diseases

ABSTRACT: Genome-wide analyses of chromatin state in human mast cells reveal molecular drivers and mediators of allergic and inflammatory diseases

PROVIDER: PRJNA518016 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8506740.fastq.gz	Fastqsanger.gz
	SRR8506750_1.fastq.gz	Fastqsanger.gz
	SRR8506750_2.fastq.gz	Fastqsanger.gz
	SRR8506760_1.fastq.gz	Fastqsanger.gz
	SRR8506760_2.fastq.gz	Fastqsanger.gz

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Comprehensive DNA Microarray Analysis for the Gene Sets Involved in Allergic Reaction by Allergic Effector Cells

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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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TGFbR signaling in squamous epithelial cells plays a fundamental role in controlling tissue specific allergic inflammation

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Project description:Best known for their roles in allergic diseases, the physiologic function of immunoglobulin E (IgE) and mast cells (the so-called allergy module of immunity) has been enigmatic. Recent evidence shows that allergic reactions can help to protect against the toxicity of venoms. As bacteria are a potent alternative source of toxins, we assessed the potential role of the allergy module in antibacterial host defense. We observed that the immune response against S. aureus skin infection includes specific IgEs and substantially improves systemic host defense against secondary S. aureus infections in mice. This acquired protection depends on functional IgE effector mechanisms and mast cells. Our results reveal the powerful antibacterial potential of the allergy module and therefore a novel physiologic function of IgEs and mast cells.

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