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Chromatin accessibility profile of Tfh cells during intestinal helminth infection

ABSTRACT: Chromatin accessibility profile of Tfh cells during intestinal helminth infection

PROVIDER: PRJNA772259 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16466356_1.fastq.gz	Fastqsanger.gz
	SRR16466356_2.fastq.gz	Fastqsanger.gz
	SRR16466357_1.fastq.gz	Fastqsanger.gz
	SRR16466357_2.fastq.gz	Fastqsanger.gz
	SRR16466358_1.fastq.gz	Fastqsanger.gz

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Chromatin accessibility profile of Tfh cells during intestinal helminth infection

Project description:The goal of this study was to define the regulation of Tfh cell response during intestinal helminth infection. Using the helminth Trichuris muris, we performed ATAC-seq analysis on Tfh cells that develop during acute vs chronic helminth infection. We found that the epigenetic profile of acute vs chronic induced Tfh cells are distinct by adopting Th2 and Th1 cell phenotypes, respectively. For example, Th2-associated genes such as the Il4 locus was more accessible in acute-induced Tfh cells (and vice versa for Th1-associated genes in chronic-induced Tfh cells).

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Transcriptomic profile of Tfh cells during intestinal helminth infection

Project description:The goal of this study was to define the regulation of Tfh cell response during intestinal helminth infection. Using the helminth Trichuris muris, we performed RNA-seq analysis on Tfh cells that develop during acute vs chronic helminth infection. We found that the transcriptomic profile of acute vs chronic induced Tfh cells are distinct and they express Th2/Th1-associated genes, respectively.

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Transcriptomic profile of Tfh cells during intestinal helminth infection

Project description:Transcriptomic profile of Tfh cells during intestinal helminth infection

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Hypoxia-inducible factor 2α promotes protective Th2 cell responses during intestinal helminth infection

Project description:Th2 cells must sense and adapt to the tissue milieu in order to provide protective host immunity and tissue repair. Here, we examined the mechanisms promoting Th2 cell differentiation and function within the small intestinal lamina propria. Single cell RNA-seq analyses of CD4+ T cells from the small intestinal lamina propria of helminth infected mice revealed high expression of the gene Epas1, encoding the transcription factor hypoxia-inducible factor 2a (HIF2α). In vitro, exposure to hypoxia or genetic HIF2α activation promoted Th2 cell differentiation, even under non-polarizing conditions. In mice, HIF2α activation in CD4+ T cells promoted intestinal Th2 cell accumulation in the absence of infection, and HIF2α-deficiency impaired CD4+ T cell-mediated host immunity to intestinal helminth infection. Our findings identified hypoxia, and the oxygen-regulated transcription factor Hypoxia-Inducible Factor 2α (HIF2α), as key regulators of Th2 cell differentiation and function within the small intestine.

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Intestinal helminth skews dendritic cell development to counter the anti-helminth immune response

Project description:Intestinal helminth skews dendritic cell development to counter the anti-helminth immune response

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Bi-directional neuro-immune communication regulates host defense against helminth infection

Project description:Emerging studies reveal that neuropeptides play critical role in regulating anti-helminth immune responses, hinting at the potential of intrinsic enteric neurons (iENs) in orchestrating intestinal immunity. However, whether and how the iENs get activated during infection, and whether they engage in a bi-directional communication with the immune cells, remain poorly defined. Here we show that iENs became activated in response to helminth infection. Single-nucleus RNA sequencing of the iENs revealed significant alterations in gene expression in IL-13R+ intrinsic primary afferent neurons (IPANs), including the upregulation of the neuropeptide -CGRP. Using genetic mouse models, we demonstrated that both group 2 innate lymphoid cells (ILC2s) and neuronal IL-13R signaling are indispensable for optimal iEN activation, which subsequently inhibit ILC2 responses and anti-helminth immunity. Together, these results reveal a previously unrecognized bi-directional neuro-immune crosstalk in the intestine.

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The prostaglandin D2 receptor CRTH2 suppresses epithelial responses during intestinal helminth infection

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