PDK1 is required for maintenance of CD4+ FoxP3+ regulatory T cell function
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ABSTRACT:
PROVIDER: PRJNA687017 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:PDK1 is required for maintenance of CD4+ FoxP3+ regulatory T cell function [heterozygous]
| PRJNA687022 | ENA
Project description:PDK1 is required for maintenance of CD4+ FoxP3+ regulatory T cell function [Hemizygous]
| PRJNA687026 | ENA
Project description:The goal of this study was to determine the effect of Treg-specific Pdpk1 (PDK1) deletion on the transcriptome of Treg cells in the absence of inflammatory conditions. CD4+ YFP+ Treg cells from spleens and peripheral lymph nodes of Cre-heterozygous Foxp3 YFP-Cre/+ Pdpk1 +/+ (WT) and Foxp3 YFP-Cre/+ Pdpk1 FL/FL (KO) were sorted, RNA was isolated and RNA-seq libraries were constructed and sequenced by Hiseq2500. Note companion data set using hemizygous Cre (induces spontaneous inflammation).
2021-02-11 | GSE163659 | GEO
Project description:The goal of this study was to determine the effect of Treg-specific Pdpk1 (PDK1) deletion on the transcriptome of Treg cells. CD4+ YFP+ Treg cells from spleens and peripheral lymph nodes of hemizygous Foxp3 YFP-Cre/0 Pdpk1 +/+ (WT) and Foxp3 YFP-Cre/0 Pdpk1 FL/FL (KO) were sorted, RNA was isolated and RNA-seq libraries were constructed and sequenced by Hiseq2000. Note companion data set using Pdpk1-deleted Treg from Cre-heterozygous mice, which do not develop spontaneous inflammation.
2021-02-11 | GSE163662 | GEO
Project description:CD4+Foxp3+ regulatory T cells (Treg) are essential for immune homeostasis and maintenance of self-tolerance. They are produced in the thymus and also generated de novo in the periphery in a TGFB dependent manner. Foxp3+ Treg are also required to achieve tolerance to transplanted tissues when induced by co-receptor or costimulation blockade. Using TCR transgenic mice to avoid issues of autoimmune pathology we show that Foxp3 expression is necessary and sufficient for tissue tolerance by coreceptor blockade. Moreover, the known need in tolerance induction for TGFB signalling to T cells, can wholly be explained by its role in induction of Foxp3, as such signalling proved dispensable for the suppressive process. We analysed the relative contribution of TGFB and Foxp3 on the transcriptome of TGFB induced Treg. TGFB elicited a large set of downregulated signature genes. The number of genes uniquely modulated due to the influence of Foxp3 alone was surprisingly limited. Retroviral conditional Foxp3 expression proved sufficient to confer transplant-suppressive potency on CD4+ T cells, and was lost once nuclear Foxp3 expression was extinguished. Thus despite the large genetic influence of TGFB exposure on iTreg the crucial Foxp3 influenced signature independent of TGFB is small. These data support a dual role for TGFB and Foxp3 in induced tolerance, where TGFB stimulates Foxp3 expression whose sustained expression is associated with acquisition of tolerance 21 samples were analyzed. 5 replicates of Marilyn.Foxp3hCD2 activated (HY)(Untreated) and TGFB-induced (HYT) cells sorted as CD4+hCD2+ and CD4+hCD2- and 3 replicates of Marilyn.Foxp3-/- activated and TGFβ-experienced (but Foxp3-) cells sorted as CD4+CD2. Pairwise comparisons were generated for the Marilyn Foxp3hCD2 UT versus TGFB induced populations and also for the Marilyn Foxp3-/- UT versus the TGFB experienced cells sorted as CD4+CD2
2012-10-03 | E-GEOD-39529 | biostudies-arrayexpress
Project description:In this study, we compared the proteomes of mouse CD4+Foxp3+ regulatory T cells (Treg) and CD4+Foxp3- conventional T cells (Tconv) in order to build a data set of proteins differentially regulated in these two cell populations. The data set contains mass spectrometry results from the analysis of 7 biological replicates of Treg/Tconv cell samples purified by flow cytometry, each experiment performed from a pool of 4-5 mice. Global proteomic analysis of each sample was performed by single-run nanoLC-MS/MS, using chromatographic separation of peptides on 50cm C18 reverse-phase columns, with either a 480min gradient on LTQ-Velos orbitrap mass spectrometer (replicates 1 and 2) or a 300min gradient on Q-Exactive orbitrap mass spectrometer (replicates 3-7). Several MS injection replicates were performed for some experiments, leading to 27 raw files composing the data set. The detailed description of each analysis (file name, sample type, biological replicate number, MS technical replicate number, MS instrument used, sample name in MaxQuant ouput) is given in the table “Files list.txt”.
2017-04-10 | PXD004436 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-02-11 | GSE163663 | GEO
Project description:CD4+Foxp3+ regulatory T cells (Treg) are essential for immune homeostasis and maintenance of self-tolerance. They are produced in the thymus and also generated de novo in the periphery in a TGFB dependent manner. Foxp3+ Treg are also required to achieve tolerance to transplanted tissues when induced by co-receptor or costimulation blockade. Using TCR transgenic mice to avoid issues of autoimmune pathology we show that Foxp3 expression is necessary and sufficient for tissue tolerance by coreceptor blockade. Moreover, the known need in tolerance induction for TGFB signalling to T cells, can wholly be explained by its role in induction of Foxp3, as such signalling proved dispensable for the suppressive process. We analysed the relative contribution of TGFB and Foxp3 on the transcriptome of TGFB induced Treg. TGFB elicited a large set of downregulated signature genes. The number of genes uniquely modulated due to the influence of Foxp3 alone was surprisingly limited. Retroviral conditional Foxp3 expression proved sufficient to confer transplant-suppressive potency on CD4+ T cells, and was lost once nuclear Foxp3 expression was extinguished. Thus despite the large genetic influence of TGFB exposure on iTreg the crucial Foxp3 influenced signature independent of TGFB is small. These data support a dual role for TGFB and Foxp3 in induced tolerance, where TGFB stimulates Foxp3 expression whose sustained expression is associated with acquisition of tolerance
2012-10-03 | GSE39529 | GEO
Project description:We previously found that NF-kB inducing kinase (NIK) overexpression in T cells via CD4 promoter driven transgene induction caused lethal autoimmunity in mice. Autoimmunity was associated with increased conventional T cell effector function and decreased regulatory T cell (Foxp3+CD4+) suppression. The goal in this study was to elucidate global transcriptional changes in Foxp3+CD4+ and Foxp3-CD4+ T cells intrinsically caused by chronic NIK overexpression in these cell types.
2016-04-29 | GSE80755 | GEO
Project description:We previously found that NF-kB inducing kinase (NIK) overexpression in T cells via CD4 promoter driven transgene induction caused lethal autoimmunity in mice. Autoimmunity was associated with increased conventional T cell effector function and decreased regulatory T cell (Foxp3+CD4+) suppression. The goal in this study was to elucidate global transcriptional changes in Foxp3+CD4+ and Foxp3-CD4+ T cells intrinsically caused by chronic NIK overexpression in these cell types. Total RNA from FACS-sorted NIKtg and WT Foxp3RFP+CD4+ and Foxp3RFP-CD4+ harvested from NIKtg/CD4Cre/Foxp3RFP + WT/Thy1.1/Foxp3RFP mixed bone marrow chimeric mice, >8 weeks after bone marrow reconstitution.
2016-04-29 | GSE80756 | GEO