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Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

ABSTRACT: Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

PROVIDER: PRJNA1013086 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25915856.fastq.gz	Fastqsanger.gz
	SRR25915857.fastq.gz	Fastqsanger.gz
	SRR25915858.fastq.gz	Fastqsanger.gz
	SRR25915859.fastq.gz	Fastqsanger.gz
	SRR25915860.fastq.gz	Fastqsanger.gz

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Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

Project description:Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

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Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

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Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

Project description:Natural killer (NK) cells are present in the circulation and can also be found residing in tissues; these populations exhibit distinct developmental requirements and are thought to differ in terms of ontogeny. Here, we investigated whether circulating conventional NK (cNK) cells can develop into long-lived, tissue-resident cells following acute infections. We found that viral and bacterial infections of the skin triggered the recruitment of cNK cells and their differentiation into Tcf1hiCD69hi tissue-resident (trNK) cells that share transcriptional similarity with CD56brightTCF1hi NK cells in human tissues. Skin trNK arose from IFN--producing effector cells and required restricted expression of the transcriptional regulator Blimp1 to optimize Tcf1-dependent trNK formation. Upon secondary infection, trNK cells rapidly gained effector function and mediated an accelerated NK cell response. Thus, cNK cells redistribute and permanently position at sites of previous infection via a mechanism promoting tissueresidency that is distinct from Hobit-dependent developmental paths of NK cells and ILC1 seeding tissues during ontogeny.

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Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

2023-12-28 | GSE242313 | GEO

Circulating NK cells establish tissue-residency upon acute infection of skin and mediate accelerated effector responses to secondary infection

Project description:Natural killer (NK) cells are present in the circulation and can also be found residing in tissues; these populations exhibit distinct developmental requirements and are thought to differ in terms of ontogeny. Here, we investigated whether circulating conventional NK (cNK) cells can develop into long-lived, tissue-resident cells following acute infections. We found that viral and bacterial infections of the skin triggered the recruitment of cNK cells and their differentiation into Tcf1hiCD69hi tissue-resident (trNK) cells that share transcriptional similarity with CD56brightTCF1hi NK cells in human tissues. Skin trNK arose from IFN-g-producing effector cells and required restricted expression of the transcriptional regulator Blimp1 to optimize Tcf1-dependent trNK formation. Upon secondary infection, trNK cells rapidly gained effector function and mediated an accelerated NK cell response. Thus, cNK cells redistribute and permanently position at sites of previous infection via a mechanism promoting tissueresidency that is distinct from Hobit-dependent developmental paths of NK cells and ILC1 seeding tissues during ontogeny

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Circulating NK cells establish tissue residency upon acute infection of skin and mediate accelerated effector responses to secondary infection.

Project description:Natural killer (NK) cells are present in the circulation and can also be found residing in tissues, and these populations exhibit distinct developmental requirements and are thought to differ in terms of ontogeny. Here, we investigate whether circulating conventional NK (cNK) cells can develop into long-lived tissue-resident NK (trNK) cells following acute infections. We found that viral and bacterial infections of the skin triggered the recruitment of cNK cells and their differentiation into Tcf1hiCD69hi trNK cells that share transcriptional similarity with CD56brightTCF1hi NK cells in human tissues. Skin trNK cells arose from interferon (IFN)-γ-producing effector cells and required restricted expression of the transcriptional regulator Blimp1 to optimize Tcf1-dependent trNK cell formation. Upon secondary infection, trNK cells rapidly gained effector function and mediated an accelerated NK cell response. Thus, cNK cells redistribute and permanently position at sites of previous infection via a mechanism promoting tissue residency that is distinct from Hobit-dependent developmental paths of NK cells and ILC1 seeding tissues during ontogeny.

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Cohesin residency determines chromatin loop patterns

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