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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity

ABSTRACT: Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity

PROVIDER: PRJNA818982 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18441627_1.fastq.gz	Fastqsanger.gz
	SRR18441627_2.fastq.gz	Fastqsanger.gz
	SRR18441628_1.fastq.gz	Fastqsanger.gz
	SRR18441628_2.fastq.gz	Fastqsanger.gz
	SRR18441629_1.fastq.gz	Fastqsanger.gz

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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity [scRNA-seq]

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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity [scRNA-seq]

Project description:Enteric helminths form intimate physical connections with the intestinal epithelium, yet their ability to directly alter epithelial stem cell fate has not been resolved. Here we demonstrate that infection of mice with the symbiotic parasite Heligmosomoides polygyrus bakeri (Hpb), reprograms the intestinal epithelium into a fetal-like state marked by the emergence of Clusterin-expressing revival stem cells (revSCs). Organoid-based studies using parasite-derived excretory/secretory products reveal that Hpb-mediated revSC generation occurs independent of host-derived immune signals and inhibits type 2 cytokine-driven differentiation of secretory epithelial lineages that promote their expulsion. Reciprocally, type 2 cytokine signals limit revSC differentiation and, consequently, Hpb fitness indicating that helminths compete with their host for control of the intestinal stem cell niche to promote continuation of their life cycle.

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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity

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