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Molecular mechanism of IgE-mediated FcεRI activation

ABSTRACT: Molecular mechanism of IgE-mediated FcεRI activation

PROVIDER: PRJNA1166917 | ENA |

REPOSITORIES: ENA

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Molecular mechanism of IgE-mediated FcεRI activation

Project description:The high-affinity Fc receptor for IgE, mainly present on mast cells and basophils, plays a crucial role in the development of allergic diseases. Monomeric IgE binding to receptor regulates mast cell survival, differentiation, and maturation. However, the underlying molecular mechanism remains unclear. Here we demonstrate that, prior to IgE binding, IgE receptor mostly exists as a homo-dimer on human mast cell membrane. The structure of human IgE receptor confirms the dimeric organization. Cholesterol-like molecules embedded within the transmembrane domain may stabilize the dimeric assembly. Upon IgE binding, the dimeric IgE receptor dissociates into two protomers, each binding to an IgE molecule. Importantly, this process elicits transcriptional activation of Egr1/3 and Ccl2 in rat basophils, which can be attenuated by inhibiting the IgE receptor dimer-to-monomer transition. Collectively, our study unveils the mechanism of antigen-independent, IgE-mediated receptor activation.

2024-11-30 | GSE278387 | GEO

Nano-silica particles synergistically IgE-mediated mast cell activation

Project description:Nano-silica particles synergistically IgE-mediated mast cell activation

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

Project description:The aim of this study was to investigate microRNA expression pattern and its functional relevance on the commitment toward mucosal differentiation and on IgE-mediated activation of mast cells. To identify microRNA genes the expression of which change during the differentiation and activation of murine primary mast cells in vitro, the putative committed progenitors (c-kit+ cells isolated on day 6 from differentiating cultures), immature mast cells (BMMC), mucosal-type mast cells (MMC), and IgE-activated mast cells were compared by Agilent microRNA array. RNA was isolated by miRNeasy (Qiagen) from: 1) c-kit+ cells, isolated from differentiating cultures (in the presence of IL3 and SCF) derived from the bone marrow using MACS column purification, 2) immature BMMCs obtained by cultivation of bone marrow cells in the presence of IL3 and SCF for 4 weeks, 3) mucosal-type mast cells by additional differentiation of immature BMMCs for 5 days by supplementation of IL9 and TGFbeta, and 4) activated mast cells by presensitization with anti-DNP IgE followed by IgE-crosslinking by DNP-antigen challenge for 2 hours. Agilent microRNA microarray was run on these experimental groups. Four biological replicates were included in every experimental group.

2011-01-01 | E-GEOD-24321 | biostudies-arrayexpress

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

2011-01-01 | GSE24321 | GEO

Fine particulate matter (PM2.5) promotes IgE-mediated mast cell activation through ROS/Gadd45b/JNK axis

Project description:Background: Mast cells play an important role in allergic responses and persistently exposure to environmental fine particulate matter (PM2.5) exacerbates allergic diseases,but the details remain elucidative. Conclusions: PM2.5 regulates ROS production through Gadd45b/MEKK4/JNK pathway, facilitating IgE-mediated mast cell activation.

2021-01-12 | GSE164537 | GEO

Fine particulate matter (PM2.5) promotes IgE-mediated mast cell activation through ROS/Gadd45b/JNK axis

Project description:Fine particulate matter (PM2.5) promotes IgE-mediated mast cell activation through ROS/Gadd45b/JNK axis

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Allergic microbial signature in IgE-mediated food allergies

Project description:Allergic microbial signature in IgE-mediated food allergies

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Next Generation Sequencing Facilitates Quantitative Analysis of IgG or IgE producing B cells

Project description:Emergence of IgE antibodies that bind allergens with high affinity is highly correlated with the severity of anaphylaxis. However, the underlying molecular mechanisms by which high-affinity IgE is generated remain poorly understood. We examined the effects of cytokines in IgE class switch using in-vitro B cell activation system

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T-5224, a selective inhibitor of c-Fos/AP-1, suppresses IgE-mediated mast cell activation†

Project description:Purpose:The goal of this study is to asses the gene expression changes in non-stimulated mast cell and anti-IgE-stimulated mast cell Methods:RBL-2H3 mRNA profiles of non-stimulated mast cell and anti-IgE-stimulated mast cell were generated by deep sequencing, in triplicate. Differential expression analysis was performed using the DESeq2(v1.4.5) with Q value ≦0.05, following the heatmap was drawn by pheatmap(v1.0.8) . Results:Compared with non-stimulated mast cell, anti-IgE-stimulated mast cell induced a robust transcriptional response, with 191 differentially expressed genes following anti-IgE treatment (116 upregulated and 75 downregulated). Among the up-regulated genes. Conclusions:Our study represents the first detailed analysis of RBL-2H3 transcriptomes, with biologic replicates, generated by RNA-seq technology.

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T-5224, a selective inhibitor of c-Fos/AP-1, suppresses IgE-mediated mast cell activation†

Project description:T-5224, a selective inhibitor of c-Fos/AP-1, suppresses IgE-mediated mast cell activation†

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