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IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy

ABSTRACT: IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy

ORGANISM(S): Mus musculus

PROVIDER: GSE179304 | GEO | 2021/07/03

REPOSITORIES: GEO

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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

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

2015-09-11 | GSE72921 | GEO

IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy

Project description:IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy

| PRJNA743090 | ENA

IL-4-BATF signaling directly modulates IL-9 producing mucosal mast cell (MMC9) function in experimental food allergy.

Project description: Not available

| S-EPMC7856198 | biostudies-literature

Induction of Interleukin-9-Producing Mucosal Mast Cells Promotes Susceptibility to IgE-Mediated Experimental Food Allergy.

Project description: Not available

| S-EPMC4618257 | biostudies-literature

Bach2-Batf interactions control Th2-type immune responses by regulating the IL-4 amplification loop

Project description:Although Bach2 plays an important role in regulating the Th2-type immune response, the underlying molecular mechanisms remain unclear. We herein demonstrate that Bach2 associates with Batf and binds to the regulatory regions of the Th2 cytokine gene loci. The Bach2-Batf complex antagonizes the recruitment of the Batf-Irf4 complex to AP-1 motifs and suppresses Th2 cytokine production. Furthermore, we found that Bach2 regulates the Batf and Batf3 expressions via two distinct pathways. First, Bach2 suppresses the maintenance of the Batf and Batf3 expression through the inhibition of IL-4 production. Second, the Bach2-Batf complex directly binds to the Batf and Batf3 gene loci and reduces transcription by interfering with the Batf-Irf4 complex. These findings suggest that IL-4 and Batf form a positive feedback amplification loop to induce Th2 cell differentiation and the subsequent Th2-type immune response, and Bach2-Batf interactions are required to prevent an excessive Th2 response.

2016-11-14 | GSE65084 | GEO

Transcription profiling of mouse wild type or Batf deficient T cells cultured under various combinations of IL-6 orTGF-beta

Project description:Wild type and Batf deficient T cells were stimulated under various combinations of IL-6 or TGF-beta.

2009-06-01 | E-MEXP-2152 | 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.

2017-06-30 | GSE95278 | GEO

Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (RNA-Seq)

Project description:Th17 cells secrete IL-17A, IL-17F, IL-21, and IL-22 cytokines that are critical in mediating inflammation and protecting the host from microorganisms infection. The basic leucine zipper transcription factor ATF-like (Batf) contributes to the transcriptional programming of multiple effector T cells, and is required for Th17 cell development. Here, we have interrogated mechanisms by which Batf promotes and stabilizes Th17 cell phenotype. We have shown that in vitro differentiated Th17 cells have increased expression of Th1 and Treg signature genes in the absence of Batf. In addition, Citrobacter rodentium infected Batf-deficient (Batf KO) mice fail to clear the infection, and that is correlated with diminished IL-17A and IL-22 cytokine production and increased Foxp3 and Ifng expression compared to WT mice. We find that Batf sustains Th17 phenotype in long-term culture conditions by suppressing Th1- and Treg-specific gene expression. Mechanistically, we reveal that Batf negatively regulates IL-2-STAT5 signaling and modulates STAT5 binding at the Ifng and Foxp3 gene loci thus suppressing Th1-Treg phenotype in Th17 cell development. Inhibition of STAT5 DNA binding activity in Batf KO Th17 cells was able to repress Ifng and Foxp3 expression compared to control-treated cells. Moreover, STAT5 cooperates with transcription factors Ets1 and Runx1 to mediate epigenetic modification and regulate gene expression. Thus, our study has revealed an essential function of Batf in modulating the IL-2-STAT5 signaling to promote and stabilize Th17 cell development.

2023-04-26 | GSE167418 | GEO

Batf stabilizes Th17 cell development via limiting STAT5 signaling pathway (ChIP-Seq)

2023-04-26 | GSE167417 | GEO

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