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Gene expression profiling of CD4+CD25+Foxp3+ regulatory T cells and CD4+CD25-Foxp3- T cells in the course of Plasmodium yoelii infection of BALB/c mice

ABSTRACT: The objective of the present study was to characterize the phenotype of CD4+CD25+Foxp3+ regulatory T cells (Tregs) in the course of parasitic Plasmodium yoelii (P .yoelii) infection of BALB/c mice. Therefore we performed microarray expression analysis of CD4+CD25+Foxp3+ Tregs isolated by FACS from spleens of non-infected mice and from spleens of mice infected with P. yoelii 3 days and 5 days post infection. By comparing the gene expression profiles, we were able to identify molecules which were differentially expressed by Tregs during parasitic infection and thereby might be involved in their immune-suppressive function. Moreover, we included CD4+CD25-Foxp3- T cells from spleens of non-infected and P. yoelii-infected mice in our analysis. It was proposed that immune-suppressive CD4+CD25-Foxp3- T cells might be induced during Plasmodium infection of mice. Thus, detailed gene expression data of these cells in comparison to CD4+CD25+Foxp3+ Tregs would contribute a better understanding in the phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE34621 | GEO | 2012/04/16

SECONDARY ACCESSION(S): PRJNA151295

REPOSITORIES: GEO

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Gene expression profiling of CD4+CD25+Foxp3+ regulatory T cells and CD4+CD25-Foxp3- T cells in the course of Plasmodium yoelii infection of BALB/c mice

Project description:The objective of the present study was to characterize the phenotype of CD4+CD25+Foxp3+ regulatory T cells (Tregs) in the course of parasitic Plasmodium yoelii (P .yoelii) infection of BALB/c mice. Therefore we performed microarray expression analysis of CD4+CD25+Foxp3+ Tregs isolated by FACS from spleens of non-infected mice and from spleens of mice infected with P. yoelii 3 days and 5 days post infection. By comparing the gene expression profiles, we were able to identify molecules which were differentially expressed by Tregs during parasitic infection and thereby might be involved in their immune-suppressive function. Moreover, we included CD4+CD25-Foxp3- T cells from spleens of non-infected and P. yoelii-infected mice in our analysis. It was proposed that immune-suppressive CD4+CD25-Foxp3- T cells might be induced during Plasmodium infection of mice. Thus, detailed gene expression data of these cells in comparison to CD4+CD25+Foxp3+ Tregs would contribute a better understanding in the phenotype. FACS sorted CD4+CD25+Foxp3+ Tregs and CD4+CD25-Foxp3- T cells from pooled spleens of non-infected Foxp3/ eGFP mice (served as reference) and from pooled spleens of P. yoelii infected Foxp3/ eGFP mice 3 days and 5 days post infection were analyzed as single probes.

2012-04-15 | E-GEOD-34621 | biostudies-arrayexpress

Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice

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Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice

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

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Project description:The concept of immune regulation/suppression has been well-established. With thymus-derived CD4 CD25 regulatory T (TR) cells, it became clear that a variety of additional peripherally induced TR cells play vital roles in protection from many harmful immune responses including intestinal inflammation. In the present study, we have analyzed in vivo-induced Ag-specific CD4 TR cells with respect to their molecular and functional phenotype. By comparative genomics we could show that these Ag-specific TR cells induced by chronic Ag stimulation in vivo clearly differ in their genetic program from naturally occurring thymus-derived CD4 CD25 TR cells. This distinct population of induced TR cells express neither CD25 nor the TR-associated transcription factor Foxp3. Strikingly, CD25 is not even up-regulated upon stimulation. Despite the lack in Foxp3 expression, these in vivo-induced CD25 TR cells are able to interfere with an Ag-specific CD8 T cell-mediated intestinal inflammation without significant increase in CD25 and Foxp3 expression. Thus, our results demonstrate that in vivo-induced Ag-specific TR cells represent a distinct population of Foxp3 CD25 TR cells with regulatory capacity both in vitro and in vivo. Keywords: cell type comparison

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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

RNAseq of bulk regulatory T cells (Tregs) and conventional T cells (Tconvs) during acute kidney injury and fibrosis development

Project description:We performed bulk RNA-seq from FACS-sorted Tregs (Foxp3+) and T convs (Foxp3-) CD4+ T cells from kidneys and spleens at different phases after injury.

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Transcription profiling of mouse Foxp3- CD25- regulatory T cells

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Phosphoproteomic analysis of T cell receptor stimulation-induced changes in human primary CD4+CD25- T cells in the absence or presence of regulatory T cells.

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.

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Profiling of naÃ¯ve and memory Tregs

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, naÃ¯ve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naÃ¯ve (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: naÃ¯ve (CD4+CD25hiCD45RA+) and memory (CD4+CD25hiCD45RA-) Tregs, and naÃ¯ve (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.

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