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IPSC-derived NK cells and anti-PD-1 antibody synergize to enhance T cell cytokine and cytolytic responses against multiple tumors

ABSTRACT: iPSC-derived NK cells and anti-PD-1 antibody synergize to enhance T cell cytokine and cytolytic responses against multiple tumors

PROVIDER: PRJNA660955 | ENA |

REPOSITORIES: ENA

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iPSC-derived NK cells and anti-PD-1 antibody synergize to enhance T cell cytokine and cytolytic responses against multiple tumors

Project description:We have developed a robust and efficient manufacturing system for the differentiation and expansion of high-quality NK cells (iNKs) derived from induced pluripotent stem cells (iPSCs). We used GeneChip microarrays to compare the whole transcriptome of iNK cells to the transcriptomes of primary T cell and NK cell populations, K562 feeder cell-expanded primary NK cells, fibroblasts, iPSCs and iCD34+ cells.

2020-11-11 | GSE157327 | GEO

Cytokine-enhanced cytolytic activity of Exosomes from NK Cells [small RNA seq]

Project description:Cytokine-enhanced cytolytic activity of Exosomes from NK Cells [small RNA seq]

| PRJNA631792 | ENA

Cytokine-enhanced cytolytic activity of Exosomes from NK Cells

Project description:Natural killer (NK) cells are a type of innate lymphocytes that play key roles in immune surveillance against tumors and viral infection. NK cells distinguish abnormal cells from healthy cells by cell-cell interaction with cell surface proteins and then attack target cells via multiple mechanisms involving TRAIL, Fas Ligand, cytokine secretion, perforin, and granzymes. In addition, extracellular vesicles (EVs), including exosomes derived from NK cells (NK-EVs), possess cytotoxic capacity against tumor cells, but their characteristics and regulation by cytokines remain unknown. Here, we report that EVs derived from human NK-92 cells stimulated with IL-15 + IL-21 show enhanced cytotoxic capacity against tumor cells in a granzyme B independent manner. In addition, small RNA-seq and mass spectrometry analyses indicate that miRNA and protein profiles in EVs are altered by cytokine stimulation. We also show NK-EVs are taken up by target cells via macropinocytosis. Collectively, our findings reveal novel characteristics of NK-EVs and the mechanism of their incorporation into target cells.

2021-09-09 | PXD018982 | Pride

Cytokine-enhanced cytolytic activity of Exosomes from NK Cells [small RNA seq]

2021-05-01 | GSE150342 | GEO

Mouse cytokine antibody array

Project description:Tumors of hematopoietic stem cell transplantation (HSCT) or control mice were collected at day 14 post transplantation. Comprehensive analysis of cytokine levels were performed by using commercially available RayBio Mouse Cytokine Array G series III and IV (RayBiotech, Inc.) according to manufacturerM-^As protocol. There are two samples: non-HSCT control group and HSCT group. Each group consists of 2 replications.

2013-08-28 | E-MTAB-1761 | biostudies-arrayexpress

Global gene expression profile of Japanese encephalitis virus(JEV) infected cytolytic B16F10 and Non-cytolytic JEV resistant B16F10r

Project description:B16F10, a murine melanoma cel line is cytolytic to JEV infection. We have identified a B16F10 cell line variant which is non-cytolytic to JEV infection. This variant cell line has two types of cells, one which is persistently infected JEV and another which is resistant to JEV infection. The JEV-resistant cells (B16F10r) were seperated from the presistently infected cells by single cell cloning. To understand the mechanism of JEV resistance microarray analysis was caried out to Identify and characterize genes differentially expressed during in uninfected/JEV-infected B16F10 and B16F10r cells. Agilent one-color experiment,Organism: Mus musculus ,Agilent Custom Mouse Whole Genome Mouse 8x60k Gene expression designed by Genotypic Technology Private Limited, Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)

2013-08-01 | E-GEOD-42942 | biostudies-arrayexpress

Cytokine induced NK memory transcriptional profile characterization

Project description:Cytokine induced NK memory transcriptional profile characterization

| PRJNA504634 | ENA

CD160 activation by herpesvirus entry mediator augments inflammatory cytokine production and cytolytic function by NK cells.

Project description: Not available

| S-EPMC3702646 | biostudies-literature

Global gene expression profile of Japanese encephalitis virus(JEV) infected cytolytic B16F10 and Non-cytolytic JEV resistant B16F10r

2013-08-01 | GSE42942 | GEO

Viral infection enhances NK cell activation via Type I dependent pathways and can be utilized to enhance influenza-specific monoclonal antibody therapies

Project description:NK cells are an essential component for the control of influenza infection, acting to both clear virus-infected cells and release antiviral cytokines. Engagement of the NK cell CD16-receptor by antibody-coated influenza-infected cells results in antibody-dependent cellular cytotoxicity (ADCC). Though NK cell-mediated ADCC is an important mechanism to control influenza, influenza infection itself may act to enhance the potency of NK cell ADCC. To understand if virus-infected cells increase NK cell activation, we co-cultured human PBMCs with influenza-infected human alveolar epithelial (A549) cells and evaluated the capacity of NK cells to mediate ADCC. Pre-incubation of PBMCs with influenza-infected target cells markedly enhanced the functionality of NK cells by ADCC antibodies in response to HA immune-complexes containing intravenous immunoglobulin (IVIG), allogenic target cells, with and without rituximab. Trans-well and supernatant transfer experiments showed that virus released into the supernatant is responsible for the enhanced functionality of NK cells, which is apparent at both the protein and RNA transcriptomic levels. Furthermore, cytokine multiplex data, RNA sequencing and cytokine blocking/supplementation experiments showed Type I interferons released from PBMCs were the primary mechanism of the influenza-induced increased NK cell functionality and ADCC potency. Importantly, the influenza infection-mediated increase in NK cell mediated anti-influenza ADCC was mimicked by the type I interferon agonist Poly-IC. This suggests a potential mechanism for enhancing monoclonal antibody therapies for influenza. We conclude that influenza-infection induced secretion of type I interferons enhances the ADCC capacity of NK cells and this pathway may potentially be manipulated to improve anti-influenza therapies.

2019-01-03 | GSE115203 | GEO

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