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RELMβ Sets the Threshold for Microbiome-Dependent Oral Tolerance

ABSTRACT: RELMβ Sets the Threshold for Microbiome-Dependent Oral Tolerance

PROVIDER: PRJNA914413 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22836030_1.fastq.gz	Fastqsanger.gz
	SRR22836030_2.fastq.gz	Fastqsanger.gz
	SRR22836031_1.fastq.gz	Fastqsanger.gz
	SRR22836031_2.fastq.gz	Fastqsanger.gz
	SRR22836032_1.fastq.gz	Fastqsanger.gz

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RELMβ Sets the Threshold for Microbiome-Dependent Oral Tolerance

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

RELMβ sets the threshold for microbiome-dependent oral tolerance.

Project description: Not available

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Project description:RELMb Sets the Threshold for Microbiome-Dependent Oral Tolerance

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Dipeptidyl peptidase 3 sets the threshold for immune activation and survival during experimental bacterial infection

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Project description:Celiac disease (CeD) is an autoimmune disorder triggered by dietary gluten. While HLA-DQ2/8-mediated presentation of gliadin peptides is required for disease, the mechanisms that underlie the loss of oral tolerance to gluten remain incompletely understood. Long noncoding RNAs (lncRNAs) have been increasingly recognized as regulators of immune function, yet their role in oral tolerance has not been previously explored. Using a screen designed to identify lncRNAs responsive to T cell activation and enriched for CeD-associated GWAS variants, we identified lnc13 as a top candidate. In HLA-DQ8 transgenic mice lacking lnc13, unmanipulated gluten ingestion led to hallmark features of loss of oral tolerance to gluten: reduced regulatory T cells, and increased IFN-γ⁺ lymphocytes, IL-12⁺ myeloid cells, cytotoxic intraepithelial immune cells and crypt hyperplasia in the small intestine. Mechanistically, lnc13 binds specific DNA regulatory regions and limits inflammatory responses to pro-inflammatory signals. In particular, lnc13 restrains IL-15-driven differentiation of CD8⁺ NK-like lymphokine-activated killer cells—an IL-15–dependent pathway strongly implicated in CeD. These findings establish lnc13 as a critical noncoding modulator of oral gluten tolerance.

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Project description:Collectively, viruses are the principal cause of cancers arising in patients with immune dysfunction, including HIV+ patients. Kaposi’s Sarcoma (KS) etiologically linked to KSHV continues to be the most common AIDS-associated tumor. The involvement of oral cavity represents one of the most common clinical manifestations of this tumor. HIV infection incurs an increased risk for periodontal diseases and oral carriage from a variety of pathogenic bacteria. In the current study, by using 16S rRNA based pyrosequencing, we found that oral shedding of KSHV altered oral microbiota signature in HIV+ patients which may contribute to virus-associated malignancies development.

2022-04-05 | GSE190132 | GEO

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