Project description:This study evaluates the genotype of NK cells sorted for expression of TIGIT into TIGIThigh, TIGITmedium and TIGITnegative NK cells. RNAseq was performed on these three NK cell populations.
Project description:To investigate differences in gene expression between bulk NK cells from naturally cycling endometrium versus bulk NK cells from superovulated endometrium, we performed bulk RNAseq of sort-purified endometrial NK cells.
Project description:The dataset contains RNAseq data from 5 subsets of NK cells isolated from human lung:
1) CD69+CD49a+CD103+CD16-CD56bright NK cells
2) CD69+CD49a+CD103-CD16-CD56bright NK cells
3) CD69+CD49a-CD103-CD16-CD56bright NK cells
4) CD69-CD49a-CD103-CD16-CD56bright NK cells
5) CD56dimCD16+NKG2A+CD57- NK cells
The dataset contains paired data for the subsets from 2 donors with 2 biological replicates/donor and subset.
Project description:We showed Cytokine induced memory-like (CIML) human NK cells have higher trasduction efficiency with CAR lentivirus for therapeutics. We performed single cell RNAseq analysis to comprehensively understand the transcripttion difference between NPM1c-CAR-mb15 CIML NK cells and CAR-negative CIML NK cells, as well as their transcriptional response to NPM1c+ AML tumor cells.
Project description:We sorted Eomes-negative NK cells (CD3- CD56+ CXCR6- CD16-) and Eomes-positive NK cells (CD3- CD56+ CXCR6+) from total leukocytes isolated from the perfusion fluid of five healthy human livers destined for transplantation. Total RNA was extracted from sorted cells, cDNA generated and RNASeq performed.
Project description:We studied the impact of DT treatment (Treg depletion) on NK cells (CD3-, NKp46+, DX5+) in axillary TDLNs and lungs of tumor bearing Foxp3GFP-DTR mice . Here we generated RNAseq data from sorted NK cells from DT or PBS treated Foxp3GFP-DTR mice bearing 100mm2 mammary tumors from lungs, axillary TDLNs
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>
Project description:We found that treatment with the TDB mosunetuzumab in patients resulted in natural killer (NK) cell activation in the peripheral blood. We modeled this phenomenon using PBMCs in vitro and found that TDB-mediated killing activated NK cells, increasing natural killing and antibody dependent cytotoxic (ADCC) function. To define TDB-mediated NK cell activation, we sorted NK cells from PBMCs at baseline and after TDB treatment and performed RNAseq.
Project description:T-bet and Eomes are related T-box transcription factors that control NK cell development. This study was designed to understand the specific roles of Eomes and T-bet in regulating gene expression. RNAseq data were generated for immature (CD11b- CD27+) and mature (CD11b+ CD27-) NK cells from T-bet KO (Tbet Ho) or control mice (Tbet WT) or from Eomes KO (Eomes Ho) or control mice (NK-Cre). Three samples were generated for each condition (Tri 1, 2, 3).
Project description:Cord blood (CB)-derived chimeric antigen receptor (CAR)-natural killer (NK) cells targeting CD19 has been shown to be effective against B cell malignancies. While human CD56+ NK cells can be expanded in vitro, it is also known that NK cells can be differentiated from hematopoietic progenitor cells. It is still unclear whether CAR-NK cells are originated from mature NK cells or NK progenitor cells in CB. Here we found that CAR-NK cells are predominantly derived from the CD56- NK progenitor cells. We first found that substantial numbers of CD19 CAR-NK cells were produced from the CD56- CB mononuclear cells after in vitro culture for two weeks. Single cell RNAseq analysis of CD56-CD3-CD14-CD19- CB mononuclear cells revealed that those cells were subdivided into three subpopulations based on the expression of CD34 and HLA-DR. NK cells were predominantly produced from the CD34-HLA-DR- cells. In addition, in the CD34-HLA-DR- cells, only CD7+ cells could differentiate into NK cells. These results indicate that CD56-CD7+CD34- HLA-DR-lineage marker (Lin)- cells are the major origin of human CB-derived CAR-NK cells, indicating that we need to develop methods to enhance the quality and quantity of NK cells produced from these NK cell progenitor cells.
