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Methylomes from naïve CD4+ T-cells from infants and children with and without food allergy [methylation]

ABSTRACT: Methylomes from naïve CD4+ T-cells from infants and children with and without food allergy [methylation]

PROVIDER: PRJNA464395 | ENA |

REPOSITORIES: ENA

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Methylomes from naïve CD4+ T-cells from infants and children with and without food allergy [methylation]

Project description:Here we studied the epigenetic regulation of the naïve CD4+ T-cell activation response among children with IgE-mediated food allergy. Using integrated DNA methylation and transcriptomic profiling, we found that food allergy in infancy is associated with dysregulation of T-cell activation genes. Reduced expression of cell cycle related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) were associated with poorer T-lymphoproliferative responses in infancy after polyclonal activation of the T-cell receptor.

2018-05-31 | GSE114134 | GEO

Transcriptomes and methylomes from naïve CD4+ T-cells from infants and children with and without food allergy

Project description:Transcriptomes and methylomes from naïve CD4+ T-cells from infants and children with and without food allergy

| PRJNA464396 | ENA

Transcriptomes from naïve CD4+ T-cells from infants and children with and without food allergy [RNA-seq]

2018-05-31 | GSE114065 | GEO

Transcriptomes from naïve CD4+ T-cells from infants and children with and without food allergy [RNA-seq]

Project description:Transcriptomes from naïve CD4+ T-cells from infants and children with and without food allergy [RNA-seq]

| PRJNA464049 | ENA

Transcriptomes and methylomes from naïve CD4+ T-cells from infants and children with and without food allergy

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

2018-05-31 | GSE114135 | GEO

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

Project description:Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy. dUTP mRNA-Seq profiles of indicated hematopoietic cell lineages were generated on Illumina HiSeq2500. Hematopoietic cells were isolated from Balb/C mice that developed food allergy and bone marrow-derived mast cells were generated from naïve Balb/C mice

2015-09-11 | E-GEOD-72921 | biostudies-arrayexpress

Skin inflammation exacerbates food allergy symptoms in epicutaneously sensitized mice

Project description:Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy. We examined whether skin barrier impairment deteriorated food allergy symptoms in epicutaneously sensitized mice. To clarify the association between skin inflammation and food allergy symptoms, we analyzed gene expression at skin lesions using a GeneChip.

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Epigenetic profiling of children with respiratory allergy

Project description:The prevalence of respiratory allergy in children is increasing. Epigenetic changes (e.g. DNA methylation) are plausible underlying molecular mechanisms. Longitudinal birth cohorts are instrumental to study the relation between early-life environmental factors and the development of complex diseases. Our AXA Research Fund and Cefic-LRI supported project explores the hypothesis that chemical exposures during pregnancy can influence the immune system and development of allergy in children. Questionnaire data, as well as cord blood, plus blood and saliva samples at age 11 years, were collected in substudies of two longitudinal birth cohorts in Belgium (FLEHS1 & FLEHS2) and analyzed with Illumina Methylation 450K BeadChips as well as gene targeted iPLEX MassArrays analysis. The project aims to answer the following questions: 1) can we identify specific changes in epigenetic modifications on DNA from allergic compared to not-allergic children; 2) are these allergy-related epigenetic changes a result of chemical exposure during pregnancy; and 3) did the early life exposures leave an epigenetic “mark” that is maintained through childhood. If chemicals exposures and resulting predictive markers of allergic diseases can be detected early, prevention strategies, particularly in children or before pregnancy, could be developed.

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DNA methylation and transcriptomic signatures in patients with peanut- and multi-food allergy (Methylation)

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