Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE6813 | GEO | 2008/12/19
SECONDARY ACCESSION(S): PRJNA99189
REPOSITORIES: GEO
Similar Datasets
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:A common method used both in vitro and in vivo, to identify Tregs in CD4+ T cells is through the characterization of surface marker CD25. Although CD25 expression is well correlated with regulatory activity in vitro, CD4+CD25+ T cells are not the only regulatory CD4+ T cells in vivo. Studies suggest that in many situations, CD4+CD25M-bM-^@M-^S T cells are as effective as CD4+CD25+ T cells in controlling T cell mediated disease. Therefore, CD25 is not a uniquely specific cell surface marker for the identification of Tregs. CD49f is an M-NM-16-integrin subunit which dimerizes with either the M-NM-2 1 or M-NM-2 4 subunit to form receptors for various laminin isoforms. We found that CD4+ T cells from NOD mice express CD49f, and old non-diabetic NOD mice had an increase of CD4+CD49f+ T cells in the spleen and peripheral lymph node when compared to both young and diabetic mice. This study was conducted to further characterize CD4+CD49f+ Treg cell subpopulation in NOD mice. It was found that CD4+CD49f+T cells possess suppressive ability and only one third of CD4+CD49f+ T cells expressing CD25. Based on the expression of CD49f and CD25, CD4+ T cells was divided into four populations , CD25+CD49f+ ,CD25+CD49f- ,CD25-CD49f+ but CD25-CD49f- are of suppressive ability, and we further found that Foxp3 expression was highly correlated with the suppressive ability of these three Treg populations. In conclusion our data indicate that CD49f marks a CD4+ CD25+ Treg subset with more potent suppression activity and identifies a CD25-CD4+ T cell population with suppression function in a Foxp3+ expression dependent manner. We divided CD4+ T cells into four populations: CD25+CD49f+, CD25+CD49f-, CD25-CD49f+, CD25-CD49f-; Microarray technology was used to determine gene expression differences among these four groups.
2012-05-09 | E-GEOD-30503 | biostudies-arrayexpress
Project description:A common method used both in vitro and in vivo, to identify Tregs in CD4+ T cells is through the characterization of surface marker CD25. Although CD25 expression is well correlated with regulatory activity in vitro, CD4+CD25+ T cells are not the only regulatory CD4+ T cells in vivo. Studies suggest that in many situations, CD4+CD25– T cells are as effective as CD4+CD25+ T cells in controlling T cell mediated disease. Therefore, CD25 is not a uniquely specific cell surface marker for the identification of Tregs. CD49f is an α6-integrin subunit which dimerizes with either the β 1 or β 4 subunit to form receptors for various laminin isoforms. We found that CD4+ T cells from NOD mice express CD49f, and old non-diabetic NOD mice had an increase of CD4+CD49f+ T cells in the spleen and peripheral lymph node when compared to both young and diabetic mice. This study was conducted to further characterize CD4+CD49f+ Treg cell subpopulation in NOD mice. It was found that CD4+CD49f+T cells possess suppressive ability and only one third of CD4+CD49f+ T cells expressing CD25. Based on the expression of CD49f and CD25, CD4+ T cells was divided into four populations , CD25+CD49f+ ,CD25+CD49f- ,CD25-CD49f+ but CD25-CD49f- are of suppressive ability, and we further found that Foxp3 expression was highly correlated with the suppressive ability of these three Treg populations. In conclusion our data indicate that CD49f marks a CD4+ CD25+ Treg subset with more potent suppression activity and identifies a CD25-CD4+ T cell population with suppression function in a Foxp3+ expression dependent manner.
2012-05-10 | GSE30503 | GEO
Project description:Changes in Treg function are difficult to quantify due to the lack of Treg-exclusive markers in humans and the complexity of functional experiments. We sorted naive and memory human Tregs and conventional T cells, and identified genes that identify human Tregs regardless of their state of activation. We developed this Treg signature using Affymetrix human genome U133A 2.0 microarrays. To generate Tregs and Tconvs in multiple states of activation, naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs were sorted from blood of 7 healthy adults and RNA was isolated ex vivo or after stimulation for 40h, promoting activation-induced FOXP3 in Tconvs. The gene-expression profile of the eight cell subsets was analyzed. 7 adult healthy control samples were sorted into 4 subsets: naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs. These were used for RNA ex vivo and after 40h stimulation with anti-CD3/CD28 beads to induce an activation phenotype.
2016-01-19 | E-GEOD-76598 | biostudies-arrayexpress
Project description:Regulatory T cells (Tregs) suppress other immune cells and are indispensable for human health, yet the molecular mechanisms of suppression remain incompletely understood. Tregs can suppress proliferation and cytokine production of CD4+CD25- conventional T cells (Tcons). We previously demonstrated that human Tregs rapidly suppress T cell receptor (TCR)-induced calcium, NFAT and NF-κB pathways in Tcons, leading to inhibition of effector cytokine transcription (Schmidt A et al., Science Signaling 2011 Dec 20;4(204):ra90. doi: 10.1126/scisignal.2002179). Due to the short time period required to induce suppression, it is probable that Tregs alter protein modifications, such as (de)phosphorylations, in suppressed Tcons to cause this inhibition of particular TCR signaling events, while de novo production of repressor proteins seems unlikely. Thus, in order to identify causative factors which initiate rapid Treg-mediated suppression of Tcons, we compared phosphoproteomes of 5 minutes TCR-stimulated responder Tcons re-isolated from cocultures with primary human Tregs with those from control cocultures (Tcons cocultured with other Tcons). In addition, we measured the basal state of the phosphoproteome in unstimulated Tcon of the same donors. In total, we provide phosphoproteomics data of primary human CD4+CD25- T cells from three human healthy donors each for (i) unstimulated Tcons, (ii) 5 minutes TCR-stimulated Tcons, (iii) 5 minutes TCR-stimulated and Treg-suppressed Tcons.
2017-08-28 | PXD004291 | Pride
Project description:Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice
| PRJNA99189 | ENA
Project description:Parental and BXD mouse lines were received from Jackson Laboratory and The Oak Ridge National Laboratory. Splenocytes were isolated and stained with anti-CD4 and anti-CD25 antibodies. CD4+ T cells were separated into CD4+CD25+ Treg and CD4+CD25- Th cells. Tregs and Th cell were collected from spleens of 31 BXD recombinant inbred strains and of the parental mouse strains DBA/2J and C57BL/6J. Gene expression was measured by microarrays. The comparative analysis of the transcriptomes from the two cell populations allowed us to identify many novel differentially expressed genes. Furthermore, the analysis of cis- and trans-expression Quantitative Trail Loci (eQTLs) showed that both common and unique regulatory mechanisms are active in the two cell types.
2011-12-15 | E-MTAB-836 | biostudies-arrayexpress
Project description:Spliced peptides have been identified in the class I major histocompatibility complex (MHC) peptidomes of several tumors and have emerged as novel autoantigens that can stimulate highly specific T cells. A special class of spliced peptides, hybrid insulin peptides (HIPs), bound to histocompatibility class II molecules are potential autoantigens in the development and progression of type 1 diabetes (T1D). Recently, our laboratory demonstrated that HIPs are formed during insulin granule degradation in crinosomes isolated from nonobese diabetic (NOD) mice. In our current work, we have expanded this study to examine crinosomes from two other nondiabetic mouse strains, B6 and B6.g7, to prove that HIP formation is a consequence of normal insulin granule degradation and is independent of T1D. During the course of this work, we discovered that modified peptides comprise a significant source of false positive HIP assignments in our bioinformatics pipeline and posited that similar factors could explain the high percentage of spliced peptides in recent mass spectrometry-based studies of various tumor immunopeptidomes. Therefore, we re-analyzed data files from two recent studies that reported a large percentage of spliced peptides and demonstrated that both analyses contain many spectra erroneously assigned to spliced peptide sequences.
2021-02-11 | PXD019819 | Pride
Project description:A single cell TCR-RNAseq data set comprised of CD4+CD8+ and CD4+ thymocytes and CD25+ Treg progenitors (TRP), Foxp3lo TRP, de novo developing Tregs and recirculating mature Tregs.
2022-05-31 | GSE195820 | GEO
Project description:Changes in Treg function are difficult to quantify due to the lack of Treg-exclusive markers in humans and the complexity of functional experiments. We sorted naive and memory human Tregs and conventional T cells, and identified genes that identify human Tregs regardless of their state of activation. We developed this Treg signature using Affymetrix human genome U133A 2.0 microarrays. To generate Tregs and Tconvs in multiple states of activation, naïve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naïve (CD4+CD25-CD45RA+) and memory (CD4+CD25-CD45RA-) Tconvs were sorted from blood of 7 healthy adults and RNA was isolated ex vivo or after stimulation for 40h, promoting activation-induced FOXP3 in Tconvs. The gene-expression profile of the eight cell subsets was analyzed.
2016-01-19 | GSE76598 | GEO