Undefined
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB49337 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR7718504_1.fastq.gz | Fastqsanger.gz | |||
| ERR7718504_2.fastq.gz | Fastqsanger.gz | |||
| ERR7719424_1.fastq.gz | Fastqsanger.gz | |||
| ERR7719424_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 45 |
Similar Datasets
Project description:A contrasting picture of co-obligate nutritional endosymbiosis in aphids
| PRJEB53397 | ENA
Project description:Interpreting methane yield and microbial dynamics during anaerobic co-digestion of cheese whey and poultry slaughterhouse wastewater
| PRJEB52199 | ENA
Project description:Genome wide expression profiling of human NK cells stimulated with K562 erythroleukemic tumor cells after four hours of NK-tumor co-culture. Responding NK cells were compared to non-responding NK cells, delineated by display of CD107 on the NK cell surface following cytotoxic granule release. We hypothesized that tumor responses would initiate rapid changes in gene expression in the NK cell that would identify new features of the anti-tumor response of NK cells. Results identify NK cell activation responses and induction of TNF superfamily molecules with immunoregulatory activity. Human peripheral blood NK cells were co-cultured with tumor target cell line K562 for 4 hours with GolgiStop (brefeldin) then stained for granule exocytosis marker CD107a / CD107b, and NK cell markers then FACS sorted for responding NK cells (CD107+) and non-responding NK cells (CD107-). Pooled donor sample comprised NK cells from 3 individuals.
2014-03-18 | E-GEOD-55977 | biostudies-arrayexpress
Project description:To profile the cell states of interacting natural killer (NK) cells and blood cancer cells, we cultured 26 different cell lines representing diverse hematologic neoplasms either alone or with NK cells derived from three healthy human donors. After 24 h co-culture, we labeled the cells from each monoculture or co-culture condition with oligonucleotide-conjugated antibodies against ubiquitously expressed surface proteins (with different oligonucleotide for each mono- or co-culture), enabling multiplexing in the scRNA-seq using the cell hashing method. We additionally performed pooled CRISPR screens with a single-cell transcriptome readout using the CROP-seq platform in blood cancer cells cultured either alone or in the presence of NK cells to study the effects of perturbing genes that influenced sensitivity to NK cell killing in genome-scale CRISPR screens.
2023-07-24 | E-MTAB-13204 | biostudies-arrayexpress
Project description:Background: Hepatitis B (HBV) and human immunodeficiency virus (HIV) co-infection is a common occurrence globally, with significant morbidity and mortality. Both viruses lead to dysregulated immune responses including changes in natural killer (NK) cells, a key component of antiviral defense and a promising target for HBV cure strategies. In this study we used high-throughput single cell analysis to explore the immune cell landscape in people with HBV mono-infection and HIV/HBV co-infection, on antiviral therapy, with emphasis on identifying the distinctive characteristics of NK cell subsets. Results: Our data show striking differences in the transcriptional programs of NK cells. HIV/HBV co-infection was characterized by an overrepresentation of adaptive, KLRC2 expressing NK cells, including a higher abundance of a chemokine enriched (CCL3/CCL4) adaptive cluster. The NK cell remodeling in HIV/HBV co-infection was reflected in enriched activation pathways shared with T cells, including CD3 phosphorylation and ZAP-70 translocation that can mediate stronger ADCC responses and a bias towards chemokine/cytokine signaling. By contrast HBV mono-infection imposed a stronger cytotoxic profile on NK cells and a more prominent signature of exhaustion with higher circulating levels of HBsAg. Mirroring the transcriptomic analysis, phenotypic alterations in the NK cell pool in co-infection were consistent with increased ‘adaptiveness’ and better capacity for ADCC compared to HBV mono-infection. Overall an adaptive NK cell signature correlated inversely with circulating levels of HBsAg and HBV-RNA in our cohort. Conlcusions: This study provides new insights into the differential transcriptional signature and functional profile of NK cells in HBV and HIV/HBV co-infection, highlighting new pathways that can be manipulated to tailor NK cell-focused approaches to advance cure strategies in the different population groups.
2024-08-01 | GSE241183 | GEO
Project description:We have previously shown that human umbilical cord blood CD34+ progenitor cells undergo in vitro differentiation into functional NK cells and that their co-culture in the presence of HOXB4 transduced stromal MS5 cells resulted in an increase in differentiated NK number. The present study was conducted to compare the stromal effect on NK lytic potential in the presence and absence of HOXB4. Our results provide evidence that HOXB4 transduced MS5 cells as compared to transduced, GFP (+) MS5 cells induced highly differentiated cytotoxic NK cells. Importantly, this difference was not due to the expression of activating NK receptors but was associated with an increased induction of granzyme B degranulation in response to stimulation with NK cell-susceptible targets. DNA microarray-based global transcriptional profiling confirmed the up-regulation of granzyme B. These findings provide further evidence that HOXB4 is a crucial regulator of NK function and that its use in generating functional NK cells with increased lytic potential may be significant for cancer immunotherapy.
2014-06-07 | E-MTAB-1710 | biostudies-arrayexpress
Project description:Purified NK cells were co-cultured with M. bovis BCG or M. tuberculosis H37Rv (1:1) in the presence of IL-2 (100U/ml) or IL-12 (10pg/ml) for 24h before trizol extraction. We used microarrays to detail the global gene expression underlying NK cell activation by mycobacteria. NK cell were isolated from the blood of 6 independent donors and activated with different mycobacteria and cytokines in order to study their transcriptional profiles according to mycobacterial virulence.
2011-07-26 | E-GEOD-30950 | biostudies-arrayexpress
Project description:Natural Killer (NK) cells are innate cytotoxic lymphocytes with adaptive immune features, including antigen-specificity, clonal expansion, and memory. As such, NK cells share many transcriptional and epigenetic programs with their adaptive CD8+ T cell siblings. Various signals ranging from antigen, co-stimulation, and proinflammatory cytokines are required for optimal NK cell responses in mice and humans during virus infection; however, the integration of these signals remains unclear. In this study, we identified the transcription factor IRF4 as a signal integrator to coordinate the NK cell response during viral infection. Loss of IRF4 was detrimental to the expansion and differentiation of virus-specific NK cells. This defect was partially attributed to the inability of IRF4-deficient NK cells to uptake nutrients required for survival and memory generation. Altogether, these data suggest IRF4 is a signal integrator that acts as a secondary metabolic checkpoint to orchestrate the adaptive response of NK cells during viral infection.
2023-08-03 | GSE235064 | GEO
Project description:<p>Natural killer (NK) cells are forced to cope with different oxygen environments even under resting conditions. The adaptation to low oxygen is regulated by oxygen-sensitive transcription factors, the hypoxia-inducible factors (HIFs). The function of HIFs for NK cell activation and metabolic rewiring remains controversial. Activated NK cells are predominantly glycolytic, but the metabolic programs that ensure the maintenance of resting NK cells are enigmatic. By combining <em>in situ</em> metabolomic and transcriptomic analyses in resting murine NK cells, our study defines HIF-1a as a regulator of tryptophan metabolism and cellular nicotinamide adenine dinucleotide (NAD+) levels. The HIF-1a/NAD+ axis prevents ROS production during oxidative phosphorylation (OxPhos) and thereby blocks DNA damage and NK cell apoptosis under steadystate conditions. In contrast, in activated NK cells under hypoxia, HIF-1a is required for glycolysis, and forced HIF-1a expression boosts glycolysis and NK cell performance <em>in vitro</em> and <em>in vivo</em>. Our data highlight two distinct pathways by which HIF-1a interferes with NK cell metabolism. While HIF-1a-driven glycolysis is essential for NK cell activation, resting NK cell homeostasis relies on HIF-1a-dependent tryptophan/NAD+ metabolism.</p><p><br></p><p><strong>Linked cross omic data sets:</strong></p><p>RNA-seq data associated with this study are available in ArrayExpress (BioStudies): accession <a href='https://www.ebi.ac.uk/biostudies/arrayexpress/studies/E-MTAB-12082' rel='noopener noreferrer' target='_blank'>E-MTAB-12082</a>.</p>
2023-06-01 | MTBLS6863 | MetaboLights
Project description:Genome wide expression profiling of human NK cells stimulated with K562 erythroleukemic tumor cells after four hours of NK-tumor co-culture. Responding NK cells were compared to non-responding NK cells, delineated by display of CD107 on the NK cell surface following cytotoxic granule release. We hypothesized that tumor responses would initiate rapid changes in gene expression in the NK cell that would identify new features of the anti-tumor response of NK cells. Results identify NK cell activation responses and induction of TNF superfamily molecules with immunoregulatory activity.
2014-03-18 | GSE55977 | GEO