Expression data from murine intestinal tissue upon depletion of regulatory T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE39351 | GEO | 2013/07/10
SECONDARY ACCESSION(S): PRJNA170685
REPOSITORIES: GEO
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Project description:Regulatory T cells (Treg) play a pivotal role in modulating immune responses and were shown to decrease atherosclerosis in murine models. How this effect is brought about remains elusive. We used microarrays to detail the global programme of gene expression in liver tissue from chimeric DEREG x Ldlr-/- mice +/- diphteria toxin enabling selective depletion of Treg. Chimeric DEREG x Ldlr-/- mice were kept on a high fat diet for 8 weeks and treated with DT (vehicle) or PBS (placebo) i.p. for 8 weeks. Upon harvest, liver tissue was ascertained from animals from both groups and a gene array was performed.
2012-12-31 | E-GEOD-36279 | biostudies-arrayexpress
Project description:Regulatory T cells (Treg) play a pivotal role in modulating immune responses and were shown to decrease atherosclerosis in murine models. How this effect is brought about remains elusive. We used microarrays to detail the global programme of gene expression in intestinal tissue from chimeric DEREG x Ldlr-/- mice +/- diphteria toxin enabling selective depletion of Treg. Chimeric DEREG x Ldlr-/- mice were kept on a high fat diet for 8 weeks and treated with DT or PBS i.p. for 8 weeks. Upon harvest, intestinal tissue was ascertained from animals from both groups and a gene array was performed.
2013-07-10 | E-GEOD-39351 | biostudies-arrayexpress
Project description:Regulatory T cells (Treg) play a pivotal role in modulating immune responses and were shown to decrease atherosclerosis in murine models. How this effect is brought about remains elusive. We used microarrays to detail the global programme of gene expression in liver tissue from chimeric DEREG x Ldlr-/- mice +/- diphteria toxin enabling selective depletion of Treg.
2012-12-31 | GSE36279 | GEO
Project description:RNA was isolated from fluorescence activated cell sorted (FACS) CD45 negative, EpCAM positive bulk tumor cells from Apcmin/+;KrasLSL-G12D/+;VillinCre; Lgr5DTReGFP;p53KO (AKVPL) intestinal tumours at different time points after a single dose of vehicle saline or diphteria toxin. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0011163
2017-03-29 | GSE92949 | GEO
Project description:Background: Regulatory T cells (Tregs) are protective in atherosclerosis but reduced during disease progression due to cell death and loss of stability. However, the mechanisms of Treg dysfunction remain unknown. Oxidized phospholipids (oxPLs) are abundant in atherosclerosis and can activate innate immune cells, but little is known regarding their impact on T cells. Given Treg loss during atherosclerosis progression and oxPL levels in the plaque microenvironment, we investigated whether oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (oxPAPC), an oxPL associated with atherosclerotic plaques, alters Treg differentiation and function. Methods: CD4+ T cells were polarized to Treg, Th1, and Th17 cells with or without oxPAPC and assessed by flow cytometry. Gene expression in oxPAPC-treated Tregs was analyzed by bulk RNA sequencing. Functional studies of oxPAPC-induced Tregs were performed by co-culturing Tregs with CTV-labeled cells in vitro, and by adoptively transferring Tregs to hyperlipidemic Ldlr-/- mice to measure atherosclerosis progression. Results: Compared to controls, oxPAPC-treated Tregs were less viable, but surviving cells expressed higher levels of the Th1-associated markers T-bet, CXCR3, and IFN-. Th1 and Th17 skewing cultures were unaltered by oxPAPC. IFN- is linked to Treg instability, thus Treg polarization experiments were repeated using Ifngr1-/- CD4+ T cells. IFNR1 deficiency did not improve cell viability in oxPAPC-treated Tregs, however, T-bet and IFN- expression was not increased in surviving cells suggesting a role for IFN-signaling. OxPAPC-treated Tregs were less suppressive in vitro, and adoptive transfer studies in hyperlipidemic Ldlr-/- mice showed that oxPAPC-induced Tregs possessed altered tissue homing and were insufficient to inhibit atherosclerosis progression. Conclusions: OxPAPC elicits Treg-specific changes altering Treg differentiation and inducing a Th1-like phenotype in surviving cells partially through IFN- signaling. This is biologically relevant as oxPAPC-treated Tregs do not reduce atherosclerosis progression in Ldlr-/- mice. This study supports the role for oxPLs in negatively impacting Treg differentiation and atheroprotective function.
2023-07-04 | GSE236226 | GEO
Project description:Analysis of Foxp3(+)epigenetics(-) T cells, Foxp3(-)epigenetics(+) T cells, and Foxp3(+)epigenetics(+) T cells. Results indicate regulatory T cell (Treg) ontogenesis requires two independent processes, expression of the transcription factor Foxp3 and establishment of Treg epigenetic programs induced by T cell receptor (TCR) stimulation. GFP+CD4+ and GFP-CD4+ splenocytes were sorted from DEREG and DEREG/Scurfy mice. These cells were activated with anti-CD3/CD28 antibodies, and then transduced with Foxp3-expressing retrovirus (pGCSamIN, NGFR marker). NGFR+ T cells sorted were subjected to microarray analysis (Affymetrix, mouse genome 430 2.0 array). To normalize the experimental conditions, Tregs (GFP+ T cells from DEREG) and Tconv (GFP- T cells from DEREG) were also activated and transduced with empty vector. Two replicates each.
2012-11-05 | E-GEOD-25252 | biostudies-arrayexpress
Project description:Intravenous Immunoglobulin (IVIg) is widely used as an immunomodulatory therapy. We have recently demonstrated that IVIg protects against airway hyper-reactivity (AHR) and inflammation in mouse models of allergic airway disease (AAD), associated with induction of Foxp3+ regulatory T cells (Treg). Using DEREG (DEpletion of REGulatory T cell) mice, in which endogenous Treg can be ablated with Diphtheria toxin (DTx) treatment, we demonstrate that IVIg generates a de novo population of induced Treg (iTreg) in the absence of endogenous Treg. IVIg-generated iTreg were sufficient for inhibition of ovalbumin-induced AHR in an antigen-driven murine model of AAD. In the absence of endogenous Treg, IVIg failed to confer protection against AHR and airway inflammation. Adoptive transfer of purified IVIg-generated iTreg prior to antigen challenge effectively prevented airway inflammation and AHR in an antigen-specific manner. The goal of this study was to characterize the gene expression profile of a pure population of IVIg-generated induced Treg (iTreg).
2016-08-10 | GSE71811 | GEO
Project description:We tried to identify growth factor(s) to promote regeneration of type 2 alveolar epitherial cells. To identify such candidates, we compared gene expression profiles of RNAs from lungs of mice of the following four different groups of bone marrow (BM) chimeric mice after diphteria toxin (DT) injection. LL, BM cells of LysM-DTR mice into LysM-DTR mice; WL, BM cells of wild-type mice into LysM-DTR mice; LW, BM cells of LysM-DTR mice into wild-type mice; WW, BM cells of wild-type mice into wild-type mice. Transcriptome analysis revealed that a set of growth factor-related genes was upregulated in the lungs of WL mice compared to LL mice.
2018-07-26 | GSE117630 | GEO
Project description:Intravenous Immunoglobulin (IVIg) is widely used as an immunomodulatory therapy. We have recently demonstrated that IVIg protects against airway hyper-reactivity (AHR) and inflammation in mouse models of allergic airway disease (AAD), associated with induction of Foxp3+ regulatory T cells (Treg). Using DEREG (DEpletion of REGulatory T cell) mice, in which endogenous Treg can be ablated with Diphtheria toxin (DTx) treatment, we demonstrate that IVIg generates a de novo population of induced Treg (iTreg) in the absence of endogenous Treg. IVIg-generated iTreg were sufficient for inhibition of ovalbumin-induced AHR in an antigen-driven murine model of AAD. In the absence of endogenous Treg, IVIg failed to confer protection against AHR and airway inflammation. Adoptive transfer of purified IVIg-generated iTreg prior to antigen challenge effectively prevented airway inflammation and AHR in an antigen-specific manner. The goal of this study was to characterize the gene expression profile of a pure population of IVIg-generated induced Treg (iTreg). Treg were isolated from mice sensitized and challenged with ovalbumin (OVA). Animals were treated with IVIg to generate iTreg with or without DTx endogenous Treg pre-depletion. Human serum albumin (HSA) was used as a control protein treatment. RNA was isolated from 4 biological replicates for each condition. 12 samples in total were hybridized to Affymetrix gene expression microarrays. variable: treatment: OVA-HSA-OVA - DTx: BMR133, BMR134, BMR135, BMR136 variable: treatment: OVA-IVIg-OVA - DTx: BMR137, BMR138, BR139, BMR140 variable: treatment: OVA-IVIg-OVA + DTx: BMR141, BMR142, BMR143, BMR144 repeat: biological replicate: eTreg: BMR133, BMR134, BMR135, BMR136 repeat: biological replicate: e_iTreg: BMR137, BMR138, BR139, BMR140 repeat: biological replicate: IVIg-iTreg: BMR141, BMR142, BMR143, BMR144
2016-08-10 | E-GEOD-71811 | biostudies-arrayexpress
Project description:Common genetic variants in a 58-kilobase (kb) region of chromosome 9p21, near the CDKN2A/B cell proliferation inhibitor genes, are strongly associated with coronary artery disease (CAD). We previously reported a congenic mouse model harboring an atherosclerosis susceptibility locus in a region of homology with the human 9p21 locus. We now report markedly decreased Cdkn2a (cyclin-dependent kinase inhibitor 2a) mRNA expression in macrophages and increased circulating levels of Ly6Chigh inflammatory monocytes in congenic mice compared to controls. A bone marrow (BM) transplantation study revealed that BM-derived cells from Cdkn2a+/- mice are capable of conferring accelerated atherosclerosis, increased inflammatory monocyte subsets and monocyte proliferation in the Ldlr-/- mouse model. These findings provide a mechanistic link between decreased expression of Cdkn2a transcripts, increased monocyte proliferation, and accelerated atherosclerosis. Aorta and macrophages from ten C57BL/6.MOLFc4(51Mb)-Ldlr-/- mice and their control C57BL/6-Ldlr-/- were obtained, RNA purified and hybridized to GPL9734 Affimetrix microarrays.
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