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.
Project description:Genome wide DNA methylation profiling study of PBMC from 71 unique primary patient blood samples. The Illumina Human Methylation 450k array was used. 29 challenge proven food allergy, 29 sensitized but oral tolerant, 13 non food allergics Mixture of food allergy phenotypes (egg allergic (15), peanut allergic (14)), food sensitization phenotypes (egg sensitized (14), peanut sensitized (15)). 4 samples had technical replicate hybridzations. Bisulphite converted DNA from the 75 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.2. Technical replicates were combined during processing, resulting in normalized Beta values for 71 unique primary patient blood samples.
Project description:It has been reported that T follicular regulatory (TFR) cells promote IgE in a food allergy model but suppress IgE in a house dust mite (HDM)-induced airway inflammation model. To understand the differential roles of TFR cells in different models, mice were sensitized with peanut plus cholera toxin (PCT) (i.g.) or challenged with HDM (i.n.). TFR cells were sorted from these mice, total RNA was extracted and used for RNA-seq. Naive mice were used as additional control.
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
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.
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
Project description:Peanut protein is a remarkably potent food allergen in susceptible individuals. The frequency of peanut allergy is approximately 1% in the US population. Peanut allergy often presents with severe symptoms, and it is seldom outgrown. We sought to understand how peanut protein activates human dendritic cells, which are crucial in promoting the activation and differentiation of pathogenic peanut-specific Th2 cells that drive allergic responses.
