Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of transcriptional profiles of (1) intestinal ILC3s isolated from WT and IL-17D-deficient mice; (2) CD93+ILC3s and CD93-ILC3s from WT mice

ABSTRACT: IL-17D/CD93 axis was essential for ILC3s hemostasis. In order to further understand how IL-17D-CD93 axis regulate ILC3s function, we conducted RNA-seq analysis of ILC3s.

ORGANISM(S): Mus musculus

PROVIDER: GSE165788 | GEO | 2021/05/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Comparison of transcriptional profiles of (1) intestinal ILC3s isolated from WT and IL-17D-deficient mice; (2) CD93+ILC3s and CD93-ILC3s from WT mice

Project description:Comparison of transcriptional profiles of (1) intestinal ILC3s isolated from WT and IL-17D-deficient mice; (2) CD93+ILC3s and CD93-ILC3s from WT mice

| PRJNA697917 | ENA

CD93+ and CD93- HSCs comparison

Project description:CD93+ and CD93- HSCs comparison

| PRJNA701025 | ENA

Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93

Project description:Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93

| PRJNA697915 | ENA

Identification of human cytotoxic ILC3s

Project description:Human ILCs are classically categorized into five subsets; cytotoxic CD127-CD94+ NK cells and non-cytotoxic CD127+CD94-, ILC1s, ILC2s, ILC3s and LTi cells. Here, we identify a novel subset within the CD127+ ILC population, characterized by the expression of the cytotoxic marker CD94. These CD94+ ILCs strongly resemble conventional ILC3s in terms of phenotype, transcriptome and cytokine production, but are highly cytotoxic. IL-15 was unable to induce differentiation of CD94+ ILCs towards mature NK cells. Instead, CD94+ ILCs retained RORγt, CD127 and CD200R expression and produced IL-22 in response to IL-15. Culturing non-cytotoxic CD127+ ILC1s or ILC3s with IL-12 induced upregulation of CD94 and cytotoxic activity, effects that were not observed with IL-15 stimulation. Thus, human helper ILCs can acquire a cytotoxic program without differentiating into NK cells.

2020-09-14 | GSE147231 | GEO

Comparison of transcriptional profiles of cultured intestinal ILC3s to freshly isolated splenic and intestinal ILC3s

Project description:ILC3s from the spleen (SP) and small intestine (SI) have been shown to be phenotypically and functional different. Intestinal factors are likely to regulate transcriptional profiles and thereby function of ILC3s. The goal of this study is to analyze if SI ILC3s acquire a SP-similar transcriptional profile after in vitro culture. Therefore transcriptional profiles of cultured SI ILC3s were compared to freshly isolated ILC3s of the murine SP and the SI by RNA seq technology. Cell suspension were generated from both organs and ILC3s (CD117+, Thy1.2+, KLRG1-, lin- (CD3, CD8, CD11b, CD11c, CD19, B220, Gr-1, TCRβ, TCRγδ, TER-119, NK1.1)) were sort purified. SI ILC3 were cultured for 7 days in vitro with IL-2, IL-7 and SCF. RNA was isolated and RNA sequencing was done using Ilumina Hiseq 2500 system and NuGEN Ovation RNA Seq System V2, with biological replicates. We show that intestinal ILC3 acquire a splenic-similar transcriptional profile after in vitro culture.

2020-03-17 | GSE114750 | GEO

CD93+ and CD93- HSCs comparison [RNA-Seq]

Project description:CD93+ and CD93- HSCs comparison [RNA-Seq]

| PRJNA701026 | ENA

CD93+ and CD93- HSCs comparison [ATAC-Seq]

Project description:CD93+ and CD93- HSCs comparison [ATAC-Seq]

| PRJNA701027 | ENA

Microarray data from human cultured ILC3s

Project description:Innate lymphoid cells (ILCs) are tissue-resident lymphocytes subdivided into ILC1s, ILC2s and ILC3s based on core regulatory programs and signature cytokines secreted. ILCs exhibit functional plasticity: for instance, human IL-22-producing ILC3s convert into IFN-γ-producing ILC1-like in vitro. Whether this conversion occurs in vivo is unclear. Using flow cytometry, mass cytometry and scRNAseq, here we found that ILC3s and ILC1s occupy opposite ends of a spectrum including discrete subsets in human tonsils. RNA velocity suggested strong directionality toward ILC1s for one ILC3-ILC1 intermediate cluster. Clonal analysis revealed graded ability of ILC3-ILC1 subsets to convert into ILC1-like cells. When examined in humanized mice, ILC3 acquisition of ILC1 features showed tissue-dependency. In chromatin studies, Aiolos emerged as a nuclear factor that cooperates with Tbet to repress evolutionarily conserved regulatory elements active in ILC3s. The human intestine also exhibited an ILC3–ILC1 transitional population. We conclude that conversion of ILC3s to ILC1-like occurs in vivo in human tissues, and that tissue factors and Aiolos are crucial for this process.

2019-06-18 | GSE132843 | GEO

Quantitative Analysis of Erythroblast Transcriptomes in Control and NUP-17d Treatment Groups

Project description:NUP-17d (17d) is an effective inhibitor of Plek2 protein. NUP-17d treatment inhibits erythroblast proliferation, differentiation and enucleation in a dose-dependent manner via directly binding to Plek2 protein. To reveal the detailed involving mechanism of NUP-17d treatment, we performed RNA sequencing to analyze the gene expression profiles change in erythroblasts which were treated with NUP-17d or DMSO (NC) for 48 hours in the EPO induction culture system.

2021-06-09 | GSE176397 | GEO

Chromatin accessibility landscapes of WT (Rag1-/-) and BATF KO (Rag1-/-Batf-/-) ILC3s sorted from small intestine [ATAC-seq]

Project description:Group 3 innate lymphoid cells (ILC3s) are crucial for the maintenance of host-microbiota homeostasis in gastrointestinal mucosal tissues. The mechanisms that maintain lineage identity of intestinal ILC3s, and ILC3s-mediated orchestration of microbiota and mucosal T cell immunity are elusive. Here, we identified BATF as a gatekeeper of ILC3s homeostasis in the gut. Depletion of BATF in ILC3s resulted in excessive interferon-γ production, dysbiosis, aberrant T cell immune responses and spontaneous inflammatory bowel disease (IBD), which was considerably ameliorated by removal of adaptive immunity or antibiotic treatment. Mechanistically, BATF directly regulates ILC3s identity by globally shapes chromatin landscape of ILC3s. BATF directly binds to the cis-regulatory elements of type 1 effector genes, restrains their chromatin accessibility and inhibits their expression. Conversely, BATF promotes chromatin accessibility of genes involved in MHCII antigen processing and presentation pathways. Collectively, our findings reveal BATF is a promising candidate to maintain ILC3s stability and coordinate ILC3s–mediated control of intestinal homeostasis.

2022-08-31 | GSE168078 | 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