Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA162393 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program. Duplicate samples of Tconv (CD3+CD4+GFP-) and Treg (CD3+CD4+GFP+) splenocytes were double-sorted to achieve > 99.0% purity, from 6 weeks old male Foxp3-Fusion-GFP and Foxp3-ires-GFP mice of both B6 and NOD backgrounds. Following cell sorting into Trizol, RNA was purified, labeled and hybridized to Affymetrix arrays.
2012-04-26 | E-GEOD-37605 | biostudies-arrayexpress
Project description:The NOD (nonobese diabetic) mouse strain develops a characteristic autoimmune syndrome that closely resembles human type I diabetes. It has been suggested that NOD mice exhibit both numerical deficiency in CD4+CD25+ regulatory T cells (Treg) and reduced suppressive activity. We compared sorted CD4+CD25+ Tregs from the spleens of 6-7 week-old female NOD and nondiabetic B6.H2g7 mice. Tregs were 93±2% and 95±1% Foxp3+ in NOD and B6.H2g7 cells, respectively, on post-sort reanalysis. "Conventional" CD4+CD25- T cells (Tconv) are included as reference populations. Surprisingly, Treg "signature" is similar between the two strains, with only a few probesets that subtly deviate. Keywords: Cell population comparison from two mouse strains. For each strain (NOD and B6.g7), we analyzed two populations: CD4+CD25+ Treg and CD4+CD25- Tconv cells, for a total of four distinct populations. RNA from three mice were pooled for each replicate; there are three independent replicates for each population. After RMA normalization, intensity values were averaged across the three replicates and analyzed. We calculated the ratio of Treg/Tconv intensity values for each strain and compared the results.
2008-12-19 | E-GEOD-6813 | biostudies-arrayexpress
Project description:Several clinical trials have shown anti-CD3 treatment to be a promising therapy for autoimmune diabetes, but its mechanism of action remains unclear. Foxp3+ regulatory T (Treg) cells are likely to be involved, and we have shown a strong effect of anti-CD3 on homeostatic control of CD4+ FoxP3+ regulatory T (Treg) cells. To analyze the early consequences of anti-CD3 treatment, we sorted and profiled Treg and conventional CD4+ T (Tconv) cells in the first hours and days after anti-CD3 treatment of NOD mice. In practice, NOD mice carrying the Foxp3-GFP reporter were treated with anti-CD3 mAb KT3 (50 ug iv) and CD4+ T cells were sorted from pooled spleen and lymph nodes after 2, 8, 24 and 72 hrs, separating Treg and Tconv cells on the basis of GFP expression. Anti-CD3 treatment led to a transient transcriptional response, terminating faster than most antigen-induced responses. Most transcripts were similarly induced in Treg and Tconv cells, but several were differential, in particular those encoding the IL7 receptor (IL7R) and transcription factors Id2/3 and Gfi1, upregulated in Treg but repressed in Tconv cells. In parallel experiments, we tested the effect of soluble anti-CD3 added to cultures of fresh splenocytes, sorting Treg and Tconv cells at the same time points. Many of the anti-CD3 elicited changes, and of the differential response observed in vivo, were also observed in vitro. Two independent replicate series; Treg and Tconv samples abbreviated TR and TC, respectively. Keywords: Transcriptional activation, TCR All gene expression profiles were obtained from highly purified T cell populations sorted by flow cytometry. RNA from 5 x 104 cells was amplified, labeled, and hybridized to Affymetrix ST1.0 Gene arrays. Raw data were preprocessed with the RMA algorithm in GenePattern, and averaged expression values were used for analysis.
2013-07-01 | E-GEOD-48210 | biostudies-arrayexpress
Project description:The NOD (nonobese diabetic) mouse strain develops a characteristic autoimmune syndrome that closely resembles human type I diabetes. It has been suggested that NOD mice exhibit both numerical deficiency in CD4+CD25+ regulatory T cells (Treg) and reduced suppressive activity. We compared sorted CD4+CD25+ Tregs from the spleens of 6-7 week-old female NOD and nondiabetic B6.H2g7 mice. Tregs were 93±2% and 95±1% Foxp3+ in NOD and B6.H2g7 cells, respectively, on post-sort reanalysis. "Conventional" CD4+CD25- T cells (Tconv) are included as reference populations. Surprisingly, Treg "signature" is similar between the two strains, with only a few probesets that subtly deviate. Keywords: Cell population comparison from two mouse strains.
2008-12-19 | GSE6813 | GEO
Project description:Several clinical trials have shown anti-CD3 treatment to be a promising therapy for autoimmune diabetes, but its mechanism of action remains unclear. Foxp3+ regulatory T (Treg) cells are likely to be involved, and we have shown a strong effect of anti-CD3 on homeostatic control of CD4+ FoxP3+ regulatory T (Treg) cells. To analyze the early consequences of anti-CD3 treatment, we sorted and profiled Treg and conventional CD4+ T (Tconv) cells in the first hours and days after anti-CD3 treatment of NOD mice. In practice, NOD mice carrying the Foxp3-GFP reporter were treated with anti-CD3 mAb KT3 (50 ug iv) and CD4+ T cells were sorted from pooled spleen and lymph nodes after 2, 8, 24 and 72 hrs, separating Treg and Tconv cells on the basis of GFP expression. Anti-CD3 treatment led to a transient transcriptional response, terminating faster than most antigen-induced responses. Most transcripts were similarly induced in Treg and Tconv cells, but several were differential, in particular those encoding the IL7 receptor (IL7R) and transcription factors Id2/3 and Gfi1, upregulated in Treg but repressed in Tconv cells. In parallel experiments, we tested the effect of soluble anti-CD3 added to cultures of fresh splenocytes, sorting Treg and Tconv cells at the same time points. Many of the anti-CD3 elicited changes, and of the differential response observed in vivo, were also observed in vitro. Two independent replicate series; Treg and Tconv samples abbreviated TR and TC, respectively. Keywords: Transcriptional activation, TCR
2013-07-01 | GSE48210 | GEO
Project description:miRNA expression profiling in highly purified murine CD4+ Tconv and Treg cells. FoxP3-GFP-hCre1a(high) reporter mice were used to separate both populations based on surface markers and presence or absence of GFP. Two-condition experiment, Tconv vs. Treg. Biological replicates: 1 Tconv, 1 Treg, purified from the same pooled mice. One replicate on 1 array.
2013-06-06 | E-GEOD-30847 | biostudies-arrayexpress
Project description:Regulatory T cells (Tregs) are responsible for limiting autoimmunity and chronic inflammation. Foxp3 is a transcription factor that acts as a master regulator of Treg development and function. A serendipitous observation led to the realization that a well-characterized Foxp3gfp reporter mouse, which expresses an N-terminal GFP-Foxp3 fusion protein, is a hypomorph that causes profoundly accelerated autoimmune diabetes on a NOD background. Although natural Treg development and in vitro function is not significantly altered in Foxp3gfp NOD and C57BL/6 mice, Treg fitness function in inflammatory environments is perturbed and TGF?-induced Treg development reduced. Foxp3gfpis unable to interact with the histone acetyltransferase Tip60, the histone deacetylase HDAC7, and the Ikaros family zinc finger 4, Eos, which leads to reduced Foxp3 acetylation and enhanced K48-linked polyubiquitylation. Collectively this leads to an altered transcriptional landscape and reduced Foxp3-mediated gene repression, notably at the hallmark IL-2 promoter. Loss of controlled Foxp3-driven epigenetic modification leads to Treg insufficiency that causes autoimmunity in prone environments. 16 samples overall split between 2 genotypes (wild type and Foxp3 knock in) and two cell types (Tregs and Tconv)
2012-12-07 | E-GEOD-35164 | biostudies-arrayexpress
Project description:Single cell VDJ and RNAseq of Tconv and Treg cells obtained from BALB/c FoxP3-GFP reporter mice
2022-11-22 | GSE180016 | GEO
Project description:miRNA expression profiling in highly purified murine CD4+ Tconv and Treg cells. FoxP3-GFP-hCre1a(high) reporter mice were used to separate both populations based on surface markers and presence or absence of GFP.
2013-06-06 | GSE30847 | GEO
Project description:The colonic lamina propria contains a distinct population of Foxp3+ T regulatory cells (Tregs) that modulate responses to commensal microbes. Analysis of gene expression revealed that the transcriptome of colonic Tregs is distinct from splenic and other tissue Tregs. Rorγ and Helios in colonic Tregs mark distinct populations: Rorγ+Helios- or Rorγ-Helios+ Tregs. We uncovered an unanticipated role for Rorγ, a transcription factor generally considered to be antagonistic to Foxp3. Rorγ in colonic Tregs accounts for a small but specific part of the colon-specific Treg signature. (1) Total colonic and splenic Foxp3+ Treg comparison: Lymphocytes were isolated from colonic lamina propria and spleens of Foxp3-ires-GFP mice, where GFP reports Foxp3 expression. TCRb+CD4+GFP+ cells were double sorted into Trizol. (2) Colonic Rorγ+ and Rorγ- Treg comparison: Foxp3-ires-Thy1.1 reporter mice were crossed to Rorc-GFP reporter mice to generate mice that report both Foxp3 and Rorγ expression. Rorγ+Foxp3+ Tregs (TCRb+CD4+Thy1.1+GFP+) and Rorγ-Foxp3+ Tregs (TCRb+CD4+Thy1.1+GFP-) from colonic lamina propria were double sorted into Trizol.To reduce variability and increase cell number, cells from multiple mice were pooled for sorting and at least three replicates were generated for all groups. RNA from 1.5-3.0 x104 cells was amplified, labeled and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.
2015-07-25 | E-GEOD-68009 | biostudies-arrayexpress