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Differential gene expression in IFNg+ and IFNg- IL-15 primed NK cells after anti-NK1.1 stimulation [IFNgReporter_RNA-seq]

ABSTRACT: Differential gene expression in IFNg+ and IFNg- IL-15 primed NK cells after anti-NK1.1 stimulation [IFNgReporter_RNA-seq]

PROVIDER: PRJNA947202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23932133_1.fastq.gz	Fastqsanger.gz
	SRR23932133_2.fastq.gz	Fastqsanger.gz
	SRR23932134_1.fastq.gz	Fastqsanger.gz
	SRR23932134_2.fastq.gz	Fastqsanger.gz
	SRR23932135_1.fastq.gz	Fastqsanger.gz

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Differential gene expression in IFNg+ and IFNg- IL-15 primed NK cells after anti-NK1.1 stimulation [IFNgReporter_RNA-seq]

Project description:We isolated splenic NK cells and cultured them for 3 days in 100 ng/ml IL-15. Next, we stimulated the cells with plate-bound anti-NK1.1 for 6 hours and sorted YFP+ (IFNg+) and YFP- (IFNg-) populations. We then performed gene expression profiling analysis using data obtained from RNA-seq from unstimulated, YFP+ or YFP- NK cells.

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Effect of IL-15 culture +/- anti-NK1.1 stimulation on splenic NK cells [mNK_IL-15_RNA-seq]

Project description:Splenic NK cells were enriched and cultured in either low dose (5-10 ng/ml) or high dose (100 ng/ml) IL-15. Naïve NKs are freshly enriched NKs, obtained the day of the anti-NK1.1 stimulation. Cells were either left unstimulated or were stimulated via plate-bound anti-NK1.1

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Effect of IL-12+IL-18 or anti-NK1.1 stimulation on splenic NK cells [mNK_Activation_RNA-seq]

Project description:We stimulated freshly enriched splenic NK cells with either IL-12+IL-18 (1ng/ml each) or plate-bound anti-NK1.1. NKs from several C57Bl/6 mice were pooled. We then performed gene expression profiling analysis using data obtained from RNA-seq at two time points: 3 or 6 hours.

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Effect of IL-15 culture +/- anti-NK1.1 stimulation on splenic NK cells [mNK_IL-15_RNA-seq]

Project description:Effect of IL-15 culture +/- anti-NK1.1 stimulation on splenic NK cells [mNK_IL-15_RNA-seq]

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Transcription profiling of mouse IFNg-primed C57BL/6 and C3H.BL6-sst1 bone-marrow macrophages infected with mycobacterium tuberculosis

Project description:Time-course transcriptional profiling of IFNg-primed C57/BL6 and C3H.BL6-sst1 bone-marrow macrophages infected with mycobacterium tuberculosis (MTB)

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Gene expression profiling of murine liver NK cells

Project description:The NK cell pool is composed of distinct NK cell subsets with divergent phenotypic and functional features. In order to determine whether DX5- and DX5+ NK cells from murine livers represent different NK cell subsets, DX5- and DX5+ liver NK cells of adult mice were respectively sorted for gene expression analysis using the Affymetrix GeneChip Mouse Genome 430 2.0 arrays. DX5-NK1.1+CD3- cells and DX5+NK1.1+CD3- cells were sorted from the liver of naive B6 wild-type mice. RNA of each sample was then extracted and hybridized on Affymetrix microarrays to detail differences between DX5- and DX5+ liver NK cells in gene expression.

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Project description:Innate Lymphoid Cells (ILCs) play a key role in tissue mediated immunity and can be controlled by co-receptor signaling. Here we define a subset of ILCs that are Tbet+NK1.1- and are present within the tumor microenvironment (TME). We show programmed death-1 receptor (PD-1) expression on ILCs within TME is found in Tbet+NK1.1-ILCs. PD-1 significantly controlled the proliferation and function of Tbet+NK1.1-ILCs in multiple murine and human tumors. We found tumor derived lactate enhanced PD-1 expression on Tbet+NK1.1-ILCs within the TME, which resulted in dampened mTOR signaling along with increased fatty acid uptake. In line with these metabolic changes, PD-1 deficient Tbet+NK1.1-ILCs expressed significantly increased IFNg, granzyme B and K. Furthermore, PD-1 deficient Tbet+NK1.1- ILCs contributed towards diminished tumor growth in an experimental murine model of melanoma. These data demonstrate that PD-1 can regulate anti-tumor responses of Tbet+NK1.1-ILCs within the tumor microenvironment.

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ADAP promotes effector cytokine release, degranulation and migration 1 of NK cells primed during in vivo Listeria monocytogenes infection in 2 mice

Project description:is involved in the formation of immune signaling complexes. To date only limited and moreover 35 conflicting data exist regarding the role of ADAP in NK cells. To extend existing knowledge we 36 investigated ADAP-dependency of NK cells in the context of in vivo infection with the intracellular 37 pathogen Listeria monocytogenes (Lm). Ex vivo analysis of infection-primed NK cells revealed 38 impaired expression of IFN-γ and chemokines as well as impaired cytotoxic capacity in NK cells 39 lacking ADAP as indicated by reduced CD107a surface expression and inefficient perforin 40 production. However, ADAP-deficiency had no global effect on NK cell morphology or intracellular 41 distribution of CD107a-containing vesicles. Proteomic definition of ADAPko and wild type NK cells 42 did not uncover obvious differences in protein composition during the steady state and moreover, 43 similar early response patterns were induced in NK cells upon infection independent of the genotype. 44 In line with protein network analyses that suggested an altered migration phenotype in naïve 45 ADAPko NK cells, in vitro migration assays uncovered significantly reduced migration of both naïve 46 as well as infection-primed ADAPko NK cells compared to wild type NK cells. We propose that this 47 migration defect might account at least in part for the fact that during in vivo infection significantly 48 lower numbers of ADAPko NK cells accumulate in the spleen i.e. the site of infection. In conclusion, 49 we show here that during systemic Lm infection in mice ADAP is essential for efficient cytokine and 50 chemokine production, cytotoxic capacity and migration of NK cells.

2020-05-27 | PXD016305 | Pride

Effect of IL-12+IL-18 or anti-NK1.1 stimulation on splenic NK cells [mNK_Activation_RNA-seq]

Project description:Effect of IL-12+IL-18 or anti-NK1.1 stimulation on splenic NK cells [mNK_Activation_RNA-seq]

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