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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse thymic T cells - Foxp3-dependent programme of regulatory T-cell differentiation (GEO Super Series0

ABSTRACT: This SuperSeries is composed of the following subset Series:; GSE7280: Gene expression in peripheral cells: effects of Foxp3 and PDE3B; GSE7770: Gene expression in thymic CD4 T cells: effects of Foxp3 Experiment Overall Design: Thymocyte RNA (GSE7770) was processed with Affy and Enzo reagents whereas peripheral cell RNA (GSE7280) was processed with Ambion reagents, which amplified the cRNA more robustly. As a result, the two data sets don't normalize very well to each other and shouldn't be compared directly to each other.

ORGANISM(S): Mus musculus

SUBMITTER: Alexander Rudensky

PROVIDER: E-GEOD-7773 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Foxp3-dependent programme of regulatory T-cell differentiation.

Gavin Marc A MA Rasmussen Jeffrey P JP Fontenot Jason D JD Vasta Valeria V Manganiello Vincent C VC Beavo Joseph A JA Rudensky Alexander Y AY

Nature 20070114 7129

Regulatory CD4+ T cells (Tr cells), the development of which is critically dependent on X-linked transcription factor Foxp3 (forkhead box P3), prevent self-destructive immune responses. Despite its important role, molecular and functional features conferred by Foxp3 to Tr precursor cells remain unknown. It has been suggested that Foxp3 expression is required for both survival of Tr precursors as well as their inability to produce interleukin (IL)-2 and independently proliferate after T-cell-rece ...[more]

PMID: 17220874

Similar Datasets

Transcription profiling of mouse peripheral T cells subsets: T-N, T-25, T-FN and T-R cells; T-25, T-FN and T-R cells after treatment with IL-2; and T-R cells transduced with empty, PDE3B-expressing or PDE3B(H801A)-expressing retroviral vectors

Project description:This data set is comprised of all peripheral (pooled lymph nodes and spleen) T cell subsets presented in this manuscript. These include T-N, T-25, T-FN and T-R cells; T-25, T-FN and T-R cells from mice treated with IL-2; and T-R cells transduced with empty, PDE3B-expressing or PDE3B(H801A)-expressing retroviral vectors (after transfer into recipient mice). Experiment Overall Design: Detailed methods are presented in the manuscript and in the attached Supplementary Information. All RNA samples were derived from cells immediately after isolation from mice. Although this data set is comprised of 2 separate experiments (cells isolated from normal mice or IL-2 treated mice and cells transduced with retroviral vectors and passaged through recipient mice), the 10 expression arrays were normalized together to allow for cross comparison.

2008-06-15 | E-GEOD-7280 | biostudies-arrayexpress

DNA binding by FOXP3 domain-swapped dimer suggests mechanisms of long-range chromosomal interactions (microarray part of this investigation)

Project description:Foxp3-mediated gene expression program in resting vs. activated CD4+ T cells The microarray part of this work consists of 12 Affymetrix assays corresponding to 3 biological replicates for each of 4 conditions for CD4+CD25- cells. Cells were either transduced with an empty vector or a vector encoding FOXP3, and in each case cells were either stimulated or not by anti-CD3/anti-CD28.

2016-09-24 | E-MTAB-4561 | biostudies-arrayexpress

CD4+ T-cell sub-populations

Project description:We investigated the transcriptome of closely related CD4+ T-cell population from healthy human donors to elucidate the processes that underly their specialized immune functions

2014-12-31 | E-MTAB-1603 | biostudies-arrayexpress

Transcription profiling of mouse natural and induced regulatory T cells

Project description:The gene expression profile of peripheral Foxp3+ natural regulatory T cells isolated from Foxp3/EGFP bicistronic mice was compared to that of in vitro-induced regulatory T cells and to CD4+ conventional (Foxp3-) T cells. The role of the regulatory T cell transcription factor Foxp3 in shaping the transcriptosomes of natural and induced regulatory T cells was analyzed using mice expressing a mutant FOXP3-EGFP fusion protein (Foxp3deltaEGFP). We used gene expression microarrays to examine the transcriptional programs of natural and induced regulatory T cells and the function of Foxp3 in organizing the transcriptosomes of the respective cell type Experiment Overall Design: Conventional T cells and natural and induced regulatory T cells were derived from Foxp3/EGFP bicistronic mice and analyzed for their gene expression profile. Conventional T cells, regulatory T cell precursors (CD4+Foxp3deltaEGFP+) and induced regulatory T cell precursors (CD4+Foxp3deltaEGFP+) cells were deriv ed from Foxp3deltaEGFP mice

2009-03-07 | E-GEOD-14415 | biostudies-arrayexpress

Human Treg LC-MSMS - Foxp3 drives oxidative phosphorylation and protection from lipotoxicity

Project description:Regulatory T cells (Treg) have been shown to adopt a catabolic metabolic programme with increased capacity for fatty acid oxidation fuelled oxidative phosphorylation (OXPHOS). The role of Foxp3 in this metabolic shift is poorly understood. Here we show that Foxp3 was sufficient to induce a significant increase in the spare respiratory capacity of the cell, the extra OXPHOS capacity available to a cell to meet increased demands on energy in response to work. Foxp3-expressing cells were enhanced in their ability to utilise palmitate for respiration and, in addition, the activity of electron transport complexes I, II and IV were enhanced following Foxp3 expression. Foxp3 also imparts a selective advantage in ATP generation capacity, one that might be exploited as a source of adenosine for functional immunomodulation. In order to explore possible mechanisms for these differences in metabolism we conducted a quantitative proteomics study to compare the contribution of TGFβ and the transcription factor Foxp3 to the Treg proteome. We used quantitative mass spectrometry to examine differences between proteomes of nuclear and cytoplasmic Foxp3-containing CD4+ T cells from various sources with Foxp3- activated CD4 T cells, as well as Treg from human peripheral blood. Gene set enrichment analysis of our proteomic datasets demonstrated that Foxp3 expression is associated with a significant up regulation of several members of the mitochondrial electron transport chain. Not only does Foxp3 influence genes directly concerned with immune function, but also with the energy generating functions of Treg.

2017-02-15 | PXD001906 | Pride

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

Gene expression analysis of iTregs and nTregs

Project description:MBP TCR Tg mouse (1B3) generates only iTregs when crossed onto RAGKO background. Tregs from 1B3.RAG mouse were used for gene expression analsysis to determine genes selectively expressed in peripherally generated iTregs iTregs from 1B3.RAG mice (>90% Foxp3+) were run against total Tregs from 1B3 and WT NOD mice. Foxp3- CD4+T cells were used as control from all strains as Tconv. (1B3 denotes MBP-TCR Tg mouse).

2013-07-03 | E-GEOD-39724 | biostudies-arrayexpress

Quantitative Proteomics Reveals Specialized Wiring of Signaling Pathways that Protects Human Regulatory T Cell Identity - 5 populations ex vivo

Project description:Regulatory CD4+ T cells (Tregs) are functionally distinct from conventional CD4+ T cells (Tconvs). To understand Treg identity, we compared by proteomics and transcriptomics human naïve (n) and effector (e)Tregs, Tconvs and transitional FOXP3+ cells. Only 12% of 422 differentially expressed proteins was identified as such at the mRNA level, demonstrating the importance of direct proteome measurement. Fifty-one proteins discriminated Tregs from Tconvs. This common Treg protein signature indicates altered signaling by TCR-, TNF receptor-, NFB-, PI3 kinase/mTOR-, NFAT- and STAT pathways, and unique cell biological and metabolic features. Another protein signature uniquely identified eTregs and revealed active cell division, apoptosis sensitivity and suppression of NFB- and STAT signaling. eTreg fate appears consolidated by FOXP3 outnumbering its partner transcription factors. These features explain why eTregs cannot produce inflammatory cytokines, whereas transitional FOXP3+ cells can. Collectively, our data reveal that Treg identity is defined and protected by uniquely “wired” signaling pathways.

2018-05-18 | PXD005477 | Pride

Quantitative Proteomics Reveals Specialized Wiring of Signaling Pathways that Protects Human Regulatory T Cell Identity - 6 populations ex vivo

2018-05-18 | PXD007744 | Pride

Transcription profiling of mouse naive CD4+CD25-CD62Lhi T cells and nTreg cells with Eos knock-down

Project description:Eos expression in Treg cells have been documented by several microarrays including ours. We hypothesized that Eos facilitates Foxp3- dependent gene repression in Regulatory T cells. In order to investigate the role of Eos in mediating the Foxp3-dependent gene silencing program, we utilized lentiviral shRNA knockdown of Eos in natural Tregs isolated from the periphery of Balb/C mice. A renilla luciferase (RL) gene specific shRNA lentivirus was used as a control for the transduction of cells. The transcriptional profile of naive T cells, natural Tregs, Eos knockdown Tregs, and control shRNA knockdown Tregs was compared using Agilent 4x 44K whole mouse genome array. The goal of this microarray is to document the global effect of the loss of Eos expression on the transcriptional profile of natrual Treg cells. Experiment Overall Design: Eos knock-down (si-Eos) was mediated by Lentivirus expressing GFP as a reporter of transduction and sorting marker. Renilla luciferase specific shRNA lentiviral transduction was carried out in parallel as a control. NaÃ¯ve (CD4+CD25-CD62Lhi) T cells and nTreg cells were freshly isolated from Balb/C mice.

2009-10-16 | E-GEOD-17166 | biostudies-arrayexpress

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