Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

8 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of mouse IFN producing killer dendritic cells

ABSTRACT: IKDCs have been newly characterized in mouse and shared functional and phenotypic properties of NK cells and dendritic cells. To formaly distinguish them from NK cells, we have performed a gene expression profile analysis of splenic and LN cell sorted IKDC and compared them with CDC and NK.We are looking for gene or group of genes specifically expressed by IKDCs and which would allow us to specifically isolate and characterize them. Experiment Overall Design: IKDC, NK and CDC were cell-sorted from spleen and lymph node (LN) of naÃ¯ve BALB/c mice (6-8 weeks).

ORGANISM(S): Mus musculus

SUBMITTER: Franck Housseau

PROVIDER: E-GEOD-11918 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Molecular characterization of murine IFN producing killer dendritic cells

Project description:IKDCs have been newly characterized in mouse and shared functional and phenotypic properties of NK cells and dendritic cells. To formaly distinguish them from NK cells, we have performed a gene expression profile analysis of splenic and LN cell sorted IKDC and compared them with CDC and NK.We are looking for gene or group of genes specifically expressed by IKDCs and which would allow us to specifically isolate and characterize them. Keywords: Freshly isolated cells

2008-06-28 | GSE11918 | GEO

Antiviral State of CD1c+ cDC associates with increased Natural Killer maturation and activation in Sjögren´s Syndrome

Project description:Primary Sjögren´s syndrome (pSS) is a heterogeneous inflammatory autoimmune disorder characterized by the infiltration of different immune subsets in exocrine glands and potential development of extra-glandular manifestations. pSS pathology and glandular tissue destruction have been linked to increased IFN responses and the induction of autoreactive T and B cells. However, association of innate immune cells such as Natural Killer (NK) cells and conventional dendritic cells (cDC) with the tissular damage and IFN environment in pSS remains understudied. Here, we identified higher expression of NKG2D, CD107a and superior cytotoxic function on circulating NK cells from pSS which was associated with significant enrichment in a subpopulation of CD16+CD56Hi NK cells in the blood of these patients. In addition, Granzyme B+ NK cells and MICab+ CD1c+ cDC could be found in proximity in tissue sections of salivary glands from pSS patients. Importantly, murine populations of CD64Hi CD11b+CD11c+ cDC and transitional NKG2Dhi CD11b+CD27+ NK1.1 cells, infiltrated in vivo into the salivary gland in a stablished pSS mouse model. Interestingly, transcriptional IFN signatures present on CD1c+ cDC from pSS are characterized by the upregulation of RIG-I and DDX60 sensors and the ISGs IFIT1 and IFIT3. These transcriptional patterns on CD1c+ cDC associated with high basal expression of MICa/b and SLAMF7 ligands for NK receptors, the Fc receptor CD64 and increased ability to induce maturation and CD107a expression in NK cells. Finally, expression of SLAMF7 and MICa/b after Poly I:C exposure was regulated by RIG-I and DDX60 on CD1c+ cDC. Therefore, crosstalk between CD1c+ cDCs and NK cells could contribute to the pathogenesis of pSS, and represent new cellular therapeutic targets for treatment of pSS.

2023-09-20 | GSE194263 | GEO

Transcription profiling of mouse resting and IL-15 activated natural killer cells

Project description:Murine NK cells were compared at rest and following 24 hours of IL-15 stimulation for their mRNA expression profiles on the Affymetrix MOE430_2 microarray platform. Additional comparators included resting bulk splenocytes. Experiment Overall Design: Three pairs of flow sorted murine NK cells (C57Bl/6) were analzyed at rest or after 24 hours of IL-15 stimulation. Three biological replicates of each condition (resting or IL-15) are included in this anlaysis. In addition, bulk resting splenocytes were used (2 biological replicates with 2 chip replicates for a total of 4 replicates).

2009-04-28 | E-GEOD-7764 | biostudies-arrayexpress

Natural killer receptor-positive innate lymphoid cells

Project description:The following lymphocytes were sorted from the lamin propria of the small intestine of EomesGfg/+ RORgtCreTGg Rosa26Yfp/+ by using the markers Lineage- CD45+ Nkp46+ NK1.1+ : 1.convential NK cells (Eomes GFP+ RORgt YFP-) 2. ILC1 (Eomes GFP- RORgt YFP-) 3. exRORgt ILC3 (Eomes GFP- RORgt YFP+). Conventional NK cells from the bone marrow (cNK BM) were sorted from Eomes Gfp/+ mice with the markers Lineage- CD45+ NK1.1+ Eomes GFP+.

2014-04-15 | E-MTAB-2428 | biostudies-arrayexpress

Extracellular vesicle-mediated communication between hepatocytes and natural killer cells promotes hepatocellular tumorigenesis

Project description:Hepatocellular carcinoma (HCC) is frequently characterized by metabolic and immune remodeling in the tumor microenvironment. We previously discovered that liver-specific deletion of fructose-1, 6-bisphphotase 1 (FBP1), a gluconeogenic enzyme ubiquitously suppressed in HCC tissues, promotes liver tumorigenesis, and induces metabolic and immune perturbations closely resembling human HCC. However, the underlying mechanisms remain incompletely understood. Here we reported that FBP1-deficient livers exhibit diminished amounts of natural killer (NK) cells and accelerated tumorigenesis. Using the diethylnitrosamine-induced HCC mouse model, we analyzed potential changes in the immune cell populations purified from control and FBP1-depleted livers and found that NK cells were strongly suppressed. Mechanistically, FBP1 attenuation in hepatocytes derepresses an EZH2-dependent transcriptional program to inhibit PKLR expression. This leads to reduced levels of PKLR cargo proteins sorted into hepatocyte-derived EVs, dampened activity of EV-targeted NK cells, and accelerated liver tumorigenesis. Our study demonstrated that hepatic FBP1 depletion promotes HCC-associated immune remodeling, partly through the transfer of hepatocyte-secreted, PKLR-attenuated EVs to NK cells.

2023-03-11 | PXD026822 | Pride

In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-γ Secretion by Natural Killer Cells

Project description:By comparing the multi-omics profile of human NK cells before and after G-CSF in vivo treatment, we identified a pathway that was activated in response to G-CSF treatment, which suppressed IFN-γ secretion in NK cells. Specifically, integrative genomic strategy uncovered that glucocorticoid receptor (GR) was activated and mediated the genomic response to G-CSF treatment in NK cells. Activated GR can inhibit secretion of IFN-γ via promoting interactions between suppressor of cytokine signaling 1 (SOCS1) promoter and enhancer and increase the expression of SOCS1.

2022-09-30 | GSE183866 | GEO

Transcription profiling by array of human CD56brightCD16-, CD56dimNKG2A+ and CD56dimNKG2A- natural killer cell subsets

Project description:CD56brightCD16-, CD56dimNKG2A+ and CD56dimNKG2A- NK cells subsets were FACS sorted and their transcriptional profile were compared after whole genome microarray analysis.

2010-08-10 | E-MEXP-2798 | biostudies-arrayexpress

Transcription profiling of mouse natural killer (NK) cell subsets defined by CD27 and CD11b expression

Project description:Previous reports have defined three subsets of mouse NK cells on the basis of the expression of CD27 and CD11b. The developmental relationship between these subsets was unclear. To address this issue, we evaluated the overall proximity between mouse NK cell subsets defined by CD27 and CD11b expression using pangenomic gene expression profiling. The results suggest that CD27+CD11b-, CD27+CD11b+ and CD27-CD11b+ correspond to three different intermediates stages of NK cell development. Experiment Overall Design: Spleen cells from RAG-/- mice have been isolated and stained with anti-NK1.1, anti CD27 and anti CD11b antibodies. NK1.1+ cells were sorted into CD27+ CD11b-, CD27+ CD11b+ and CD27- CD11b+ subsets by flow cytometry. There are two independent replicates for each sample. Total RNA was extracted with the RNeasy microkit (Qiagen) and gene expression profiles were performed according to manufacturer instructions (Affymetrix mouse 430 2.0).

2009-03-21 | E-GEOD-13229 | biostudies-arrayexpress

Transcriptome analysis of human Natural Killer (NK) cells expressing a RUNX2-specific shRNA.

Project description:Research has already gained much insight into the roles of various members of the RUNX family of transcription factors in the development of human T- and B-cells, however the importance in human NK cell development remains unclear. Therefore, we transduced a shRNA that specifically binds to all known RUNX2 isoforms in human umbilical cord blood-derived hematopoietic progenitor cells (HPC) and cultured them in vitro in an NK cell differentiation model. On day 21 of culture (CD56+CD94+) NK cells from shRNA and control cultures were sorted, after which mRNA was isolated and transcriptome analysis was performed by RNA sequencing. Evaluation of the transcriptome in these NK cells could reveal the molecular mechanisms of RUNX2.

2022-06-03 | GSE172435 | GEO

In vivo G-CSF Treatment Activates GR-SOCS1 Axis Suppressing IFN-γ Secretion by Natural Killer Cells [CUT&TAG]

Project description:Natural killer (NK) cells are lymphocytes of the innate immune system that are involved in controlling tumors or microbial infections through the production of interferon gamma (IFN-γ). Granulocyte-colony stimulating factor (G-CSF) inhibits IFN-γ secretion by NK cells, but the mechanism underlying this effect remains unclear. Here, by comparing the multi-omics profiles of human NK cells before and after in vivo G-CSF treatment, we identified a pathway that was activated in response to G-CSF treatment, which suppressed IFN-γ secretion in NK cells. Specifically, our integrative genomic strategy revealed glucocorticoid receptor (GR) activation in NK cells that mediated the genomic response to G-CSF treatment. Activated GRs can inhibit secretion of IFN-γ by promoting interactions between suppressor of cytokine signaling 1 (SOCS1) promoter and enhancer, as well as increase the expression of SOCS1. Experiments in mice confirmed that G-CSF in vivo treatment significantly down-regulated IFN-γ secretion and up-regulated GR and SOCS1 expression in NK cells. In addition, GR blockade (RU486) significantly reversed the effects of G-CSF, demonstrating that GR up-regulates SOCS1 and inhibits the production of IFN-γ by NK cells.

2022-09-14 | GSE205824 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data