Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Altre-WT and Altre-KO]

ABSTRACT: To investigate the cooperative function Altre in the regulation of Tregs with aging, we established Altre CD4-CRE and Foxp3-CRE mice in which Altre has been knockout in CD4+ T cells or Tregs.

ORGANISM(S): Mus musculus

PROVIDER: GSE227799 | GEO | 2023/05/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Young Treg]

Project description:We then performed gene expression profiling analysis using data obtained from RNA-seq of young Altre-WT and Altre-KO Tregs.

2023-05-19 | GSE229374 | GEO

RNA-seq analysis of transcriptomes of WT and Foxp3∆2 Treg cells in spleen and LNs

Project description:We performed RNA-seq analysis of Tregs isolated from Foxp3RFP/∆2Foxp3∆CNS1-cre-Thy1.1Rosa26LSL-YFP female mice. CD4+YFP+RFP+ (WT Tregs) and CD4+YFP+RFP- (Foxp3∆2 Tregs) cells were sorted from lymph nodes and spleen to a typical purity of >95% We detected 638 differentially expressed genes (DEGs, FDR < 0.05) between Foxp3∆2 and WT Tregs

2023-07-01 | GSE208094 | GEO

RNA-seq analysis of transcriptomes of WT and Foxp3∆2 Treg cells in colon lamina propria

Project description:We performed RNA-seq analysis of Tregs isolated from Foxp3RFP/∆2Foxp3GFP-cre female mice. CD4+GFP+RFP+ (WT Tregs) and CD4+GFP+RFP- (Foxp3∆2 Tregs) cells were sorted from colon lamina propria to a typical purity of >95%. In order to obtain enough RNA for sequencing, we combined the cells sortd from the cLP of three mice for library construction. Genes that were upregulated (532 genes) and downregulated (497 genes) in Foxp3∆2 Tregs

2023-11-19 | GSE208370 | GEO

Transcriptome data (mRNA and non-coding RNAs) of Bim-deficient Treg cells and aged Treg cells, respectively

Project description:CD4+YFP+ Treg cells were sorted from the peripheral lymph nodes and spleens of Foxp3-Cre mice (8-10-weeks-old), Foxp3-Cre;Bim-fl/fl mice (8-10-weeks-old), or Foxp3-Cre mice (older than 18-months-old), respectively. Detailly, peripheral lymph nodes and spleens were harvested from mice, and grinded into single cells, then the CD4+-T cells were isolated by Mouse CD4 T Lymphocyte Enrichment Set-DM (BD Biosciences, 558131), followed with FACS sorting (SONY Cell Sorter, SH800S) to purify CD4+YFP+ Treg cells with purities >99%. RNA samples were prepared with the miRNeasy Mini Kit (Qiagen, 21704), then reverse transcribed, amplified, labeled (Affymetrix GeneChip pico kit, 703308), and hybridized to Clariom D Arrays, mouse (Affymetrix, 902931).

2023-05-24 | GSE233231 | GEO

PPARγ is a major driver of the accumulation and phenotype of adipose-tissue Treg cells

Project description:This SuperSeries is composed of the following subset Series: GSE37532: Gene expression profile of regulatory T cells (Tregs) isolated from visceral adipose tissue and lymph nodes of mice sufficient and deficient of Pparg expression in Tregs GSE37533: Expression data of Pioglitazone- or vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+/- Pparg1 (or Pparg2) GSE37534: Expression data of Pioglitazone-, Rosiglitazone-, GW1929- and vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+Pparg1 Refer to individual Series

2012-05-03 | E-GEOD-37535 | biostudies-arrayexpress

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver [Naive T cells, Th17 and Tregs]

Project description:We then performed gene expression profiling analysis using data obtained from RNA-seq of Naive T cells, Th17 and Tregs.

2023-05-19 | GSE227837 | GEO

Histone/Protein Deacetylase-6, -9, and Sirtuin-1 Control Foxp3+ Treg Through Shared and Isotype-Specific Mechanisms

Project description:Targeting histone/protein deacetylase (HDAC)-6, -9, or Sirtuin-1 (Sirt1) augments the suppressive functions of Foxp3+ T regulatory (Treg) cells, but it is unclear if this involves different mechanisms, such that combined inhibition would be beneficial. We compared the suppressive functions of Tregs from wild-type C57BL/6 mice or mice with global (HDAC6-/-, HDAC9-/-, dual HDAC6/9-/-) or conditional deletion (CD4-Cre or Foxp3-Cre and floxed Sirt1; GSE26425) alone, or after treatment with isoform-selective HDAC inhibitors (HDACi). We found the heat shock response was crucial in mediating the effects of HDAC6, but not Sirt1 inhibition. Furthermore, while HDAC6, HDAC9 and Sirt1 all deacetylate Foxp3, each has diverse effects on Foxp3 transcription, and loss of HDAC9 is associated with stabilization of Stat5 acetylation and its transcriptional activity. Targeting different HDAC can increase Treg function by multiple and additive mechanisms, indicating the therapeutic potential for combinations of HDACi in the management of autoimmunity and alloresponses post-transplant. RNA from three independent samples of magnetically separated CD4+CD25+ Treg of HDAC9-/- mice, compared to wild type (C57BL/6) control.

2012-06-20 | E-GEOD-36095 | biostudies-arrayexpress

The chromatin-modifying enzyme Ezh2 is a CD28-dependent molecule critical for the maintenance of Treg identity

Project description:Regulatory T cells (Tregs) are essential for maintaining proper immune homeostasis. Extracellular signals (e.g. TCR, CD28, IL-2R) are necessary for the generation and maintenance of Tregs, but how these signals are integrated to control the gene expression patterns of Tregs is less clear. Here we show that the epigenetic regulator, Ezh2, was induced by CD28 costimulation and Ezh2 activity was elevated in Tregs as compared to conventional CD4+ T cells. Deletion of Ezh2 in mouse Tregs led to a progressive autoimmune disease because Tregs were compromised after activation, losing proper control of essential Treg lineage genes and adopting a gene expression pattern similar to Foxp3-deficient ‘Tregs.’ Lineage-tracing of Ezh2-deficient Tregs in vivo confirmed that the cells were destabilized selectively in activated Treg populations, which led to a significant loss of Tregs in non-lymphoid tissues. These studies reveal an essential role for Ezh2 in the maintenance of Treg “identity” during cellular activation and differentiation. RNAseq of sorted populations of CD62Lhi or CD62Llo Tregs for both Ezh2-HET (Foxp3YFP-Cre/Foxp3WT;Ezh2fl/+ female mice) and Ezh2-KO (Foxp3YFP-Cre/Foxp3WT;Ezh2fl/fl female mice) were generated, in triplicate for each condition, using Illumina HiSeq 2500 single-end 50bp sequencing platform.

2015-02-09 | E-GEOD-58998 | biostudies-arrayexpress

A Treg specific long non-coding RNA maintains immune-metabolic homeostasis in ageing liver

Project description:To find specific transcription factors (TFs) interact with Altre to regulate target gene expression by Cis- or Trans- action on chromatin.

2023-05-18 | PXD041040 | Pride

Steroid nuclear receptor coactivator 2 controls immune tolerance by promoting induced Treg differentiation via upregulating Nr4a2

Project description:Purpose:Steroid nuclear receptor coactivator 2 (SRC2) is a member of family of transcription co-activators. While SRC1 inhibits the differentiation of regulatory T cells (Tregs) critical for establishing immune tolerance, we show here that SRC2 stimulates Treg differentiation. SRC2 is dispensable for the development of thymic Tregs, whereas naïve CD4+ T cells from mice deficient of SRC2 specific in Tregs (SRC2fl/fl/Foxp3YFP-Cre) display defective Treg differentiation. Furthermore, the aged SRC2fl/fl/Foxp3YFP-Cre mice spontaneously develop autoimmune phenotypes including enlarged spleen and lung inflammation infiltrated with IFNγ-producing CD4+ T cells. SRC2fl/fl/Foxp3YFP-Cre mice also develop severer experimental autoimmune encephalomyelitis (EAE) due to reduced Tregs. Mechanically, SRC2 recruited by NFAT1 binds to the promoter and activates the expression of Nr4a2 which then stimulates Foxp3 expression to promote Treg differentiation. Members of SRC family co-activators thus play distinct roles in Treg differentiation and are potential drug targets for controlling immune tolerance

2022-04-30 | GSE201431 | 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