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Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures [RNA-seq]

ABSTRACT: Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures [RNA-seq]

PROVIDER: PRJNA534526 | ENA |

REPOSITORIES: ENA

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Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures

Project description:Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures

| PRJNA534523 | ENA

Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures [Nanostring]

Project description:Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures [Nanostring]

| PRJNA532851 | ENA

Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures [Nanostring]

Project description:An emerging cellular immunotherapy for cancer is based on the cytolytic activity of natural killer (NK) cells against a wide range of tumors. Although in vitro activation or ‘priming’ of NK cells by exposure to pro-inflammatory cytokines such as interleukin (IL)-2 has been extensively studied, the biological consequences of NK cell activation in response to target cell interactions are less characterized. Herein, we investigate the consequences of co-incubation with K562, CTV-1, Daudi and RPMI-8226 tumor cell lines on the phenotype, cytokine expression profile and transcriptome of human NK cells. We observe the downregulation of several activation receptors including CD16, CD62L, C-X-C chemokine receptor (CXCR)-4, natural killer group 2 member D (NKG2D), DNAX accessory molecule (DNAM)-1 and NKp46 following tumor-priming. Although this NK cell phenotype is typically associated with NK cell dysfunction in cancer, we show upregulation of NK cell activation markers such as CD69 and CD25, secretion of pro-inflammatory cytokines including macrophage inflammatory proteins (MIP-1) α /β and IL-1β/6/8 and overexpression of numerous genes associated with enhanced NK cell cytotoxicity and immunomodulatory functions such as FAS, TNFSF10, MAPK11, TNF and IFNG. Key signaling molecules exclusively affected by tumor-priming include MAP2K3, MARCKSL1, STAT5A, and TNFAIP3, which are specifically associated with NK cell cytotoxicity against tumor targets. Collectively, these findings help define the phenotypic and transcriptional signature of NK cells following their encounter with tumor cells, independent of cytokine stimulation, and provide insight into tumor-specific NK cell responses to inform the transition towards harnessing the therapeutic potential of NK cells in cancer.

2019-06-12 | GSE129800 | GEO

Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures [RNA-seq]

2019-06-12 | GSE130284 | GEO

Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures.

Project description: Not available

| S-EPMC6594622 | biostudies-literature

Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-11 | GSE130286 | GEO

Deconvoluting global cytokine signaling networks in natural killer cells

Project description:Deconvoluting global cytokine signaling networks in natural killer cells

| PRJNA588077 | ENA

Deconvoluting global cytokine signaling networks in natural killer cells

Project description:Deconvoluting global cytokine signaling networks in natural killer cells

| PRJNA688915 | ENA

Deconvoluting global cytokine signaling networks in natural killer cells [RNA-seq]

Project description:Cytokine signaling via signal transducer and activator of transcription (STAT) proteins is crucial for optimal antiviral responses of natural killer (NK) cells. However, the pleiotropic effects of both cytokine and STAT signaling preclude the ability to precisely attribute molecular changes to either source. In this study, we employ a multi-“omics” approach to deconstruct and rebuild the complex interaction of three major STAT signaling pathways in NK cells. We uncover a global STAT4-STAT5 cooperative axis that is distinct and sometimes antagonistic to the STAT1 axis. We generate a network of STAT targets that highlights an integrated negative feedback loop, and demonstrate distinct STAT modes of epigenetic regulation. Finally, we identify shared signatures between mouse in vitro profiles and profiles from viral infection and humans, highlighting clinically translatable targets. Overall, we begin to unravel the intricate crosstalk between cytokine signaling pathways, and offer a valuable resource for improving cellular immunotherapy.

2021-03-21 | GSE164115 | GEO

Deconvoluting global cytokine signaling networks in natural killer cells [RNA-Seq]

2021-04-29 | GSE140035 | GEO

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