Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1181263 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RELMβ Sets the Threshold for Microbiome-Dependent Oral Tolerance
| PRJNA914413 | ENA
Project description:Tolerance to dietary antigens is critical to avoid deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens is poorly understood. Here we demonstrate that the goblet cell-derived resistin-like molecule beta (RELMb) is a critical regulator of oral tolerance. We find that RELMb is abundant in serum in both food allergic patients and mouse models of FA. Deletion of RELMβ protects mice from FA, development of food antigen specific IgE and anaphylaxis. RELMb disrupts food tolerance through modulation of the gut microbiome by suppressing gut Lactobacilli. Tolerance is maintained via local production of indole derivatives driving FA protective RORgt+ regulatory T (Treg) cells via activation of the aryl hydrocarbon receptor (AhR). RELMb antagonism in the peri-weaning period restored oral tolerance and protected genetically prone offspring from developing FA later in life. Together, our data identify RELMb as mediating both a novel gut immune-epithelial circuit regulating tolerance to food antigens, a new mode of innate control of antigen specific adaptive immunity via microbiome editing and targetable candidates in this circuit for prevention and treatment of FA.
2022-12-27 | GSE221462 | GEO
Project description:HuMiChip was used to analyze human oral and gut microbiomes, showing significantly different functional gene profiles between oral and gut microbiome. The results were used to demonstarte the usefulness of applying HuMiChip to human microbiome studies.
2014-02-04 | E-GEOD-54290 | biostudies-arrayexpress
Project description:Microbiome regulation of lipid metabolism Germfree male C57BL/6J mice were purchased at 8 weeks of age from Charles River Laboratories (L'Arbresle, France). Mice were treated with 10^8 CFU/mL E. coli M8 strain (isolated from the feces of an ob/ob mouse) in drinking water for 14 days. At the end of the treatment, mice were subjected to an oral lipid tolerance test (OLTT) (with 6ml/kg of corn oil) after overnight fasting (14h). All mice were sacrificed 6 hours after the lipid tolerance test and ileum samples were collected for further analysis.
2017-11-08 | GSE99018 | GEO
Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬â cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11bâ cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Four dendritic cell subpopulations from mouse mesenteric lymphnodes were sorted and compared in their gene expression profile
2016-03-28 | E-GEOD-77303 | biostudies-arrayexpress
Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬– cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11b– cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development.
2016-03-28 | GSE77304 | GEO
Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬– cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11b– cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development.
2016-03-28 | GSE77303 | GEO
Project description:Oral tolerance prevents pathological inflammatory responses towards innocuous foreign antigens via peripheral regulatory T cells (pTreg cells). However, whether a particular subset of antigen-presenting cells (APCs) is required during dietary antigen exposure to instruct naïve CD4+ T cells to differentiate into pTreg cells has not been defined. Using myeloid lineage-specific APC depletion in mice, we found that monocyte-derived APCs are dispensable, while classical dendritic cells (cDCs) are critical for pTreg cell induction and oral tolerance. CD11b¬â?? cDCs from the gut-draining lymph nodes efficiently induced pTreg cells, and conversely, loss of IRF8-dependent CD11bâ?? cDCs impaired their polarization, although oral tolerance remained intact. These data reveal the hierarchy of cDC subsets in pTreg cell induction and their redundancy during oral tolerance development. Sorted naïve CD45.1 OT-II CD4 T cells were co-cultured with four dendritic cell subpopulations sorted from mouse mesenteric lymphnodes. 24h later OT-II cells were sorted again and compared in their gene expression profile.
2016-03-28 | E-GEOD-77304 | biostudies-arrayexpress
Project description:HuMiChip was used to analyze human oral and gut microbiomes, showing significantly different functional gene profiles between oral and gut microbiome.
2014-02-04 | GSE54290 | GEO
Project description:Opioid analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit long term use. In the current study using a chronic morphine-murine model a longitudinal approach was undertaken to investigate the role of morphine modulation of gut microbiome as a mechanism contributing to the negative consequences associated with opioids use. The results revealed a significant shift in the gut microbiome and metabolome within 24 hours following morphine treatment when compared to placebo. Morphine induced gut microbial dysbiosis exhibited distinct characteristic signatures profiles including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance. Collectively, these results reveal opioids-induced distinct alteration of gut microbiome, may contribute to opioids-induced pathogenesis. Therapeutics directed at these targets may prolong the efficacy long term opioid use with fewer side effects.
2018-04-16 | E-MTAB-5550 | biostudies-arrayexpress