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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

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

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

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

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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

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

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2012-06-20 | E-GEOD-36095 | 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.

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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.

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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

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