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Expression data from DC-induced Hopx-deficient and sufficient regulatory T cells after immunization

ABSTRACT: We found that Hopx is required for the function of DC-induced regulatory T cells in vivo. We used microarrays to identify relevant Hopx-targets in such cells after antigenic re-challenge in vivo. CD25/Foxp3 double positive DC-induced Hopx-deficient and sufficient regulatory T cells were FACS sorted to high purity

ORGANISM(S): Mus musculus

SUBMITTER: Daniel Hawiger

PROVIDER: E-GEOD-23167 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The transcription cofactor Hopx is required for regulatory T cell function in dendritic cell-mediated peripheral T cell unresponsiveness.

Hawiger Daniel D Wan Yisong Y YY Eynon Elizabeth E EE Flavell Richard A RA

Nature immunology 20100829 10

Induced regulatory T cells (iT(reg) cells) can be generated by peripheral dendritic cells (DCs) that mediate T cell unresponsiveness to rechallenge with antigen. The molecular factors required for the function of such iT(reg) cells remain unknown. We report a critical role for the transcription cofactor homeodomain-only protein (Hop; also known as Hopx) in iT(reg) cells to mediate T cell unresponsiveness in vivo. Hopx-sufficient iT(reg) cells downregulated expression of the transcription factor ...[more]

PMID: 20802482

Similar Datasets

Expression data from DC-induced Hopx-deficient and sufficient regulatory T cells after immunization

Project description:We found that Hopx is required for the function of DC-induced regulatory T cells in vivo. We used microarrays to identify relevant Hopx-targets in such cells after antigenic re-challenge in vivo.

2010-08-29 | GSE23167 | GEO

Persistence of effector memory Th1 cells is regulated by the homeobox only protein Group1 Hopx-/-, Group2 Hopx+/-, Group3 Hopx+/+

Project description:Hopx appears to be needed for persistence of Th1 effector memory cells. IFN-gamma-producing Th cells are significantly reduced in Hopx-deficient mice compared to Hopx-expressing littermates and Hopx-deficient Th1 cells show a defective persistence upon adoptive transfer. Moreover, Hopx protects Th1 cells from Fas-mediated cell death in vitro. To further dissect the role of Hopx and to identify target genes of Hopx, we have performed transcriptome analysis to compare gene expression in Hopx-deficient versus Hopx-competent Th1 cells. In agreement with the role of Hopx in supporting survival of Th1 effector memory cells, anti-apoptotic cells were up-regulated and pro-apoptotic genes were down-regulated in Hopx-competent compared to Hopx-deficient Th1 cells.

2010-09-30 | GSE24437 | GEO

Next generation sequencing for quantitative transcriptomic analysis of Hopx-wildtype and Hopx-knockout murine bone marrow cells.

Project description:We generated Hopx conditional knockout mouse (Hopx-/-) and studied the biological effects of Hopx knockout on the hematopoietic system, via whole-transcriptome RNA-seq. The findigns of our studies support crucial roles of Hopx in physiological and malignant hematopoiesis.

2023-02-18 | GSE145476 | GEO

Next generation sequencing for quantitative transcriptomic analysis of subpopulations of BM cells from young Hopx-wildtype and Hopx-knockout mice.

Project description:Hopx conditional knockout mouse (Hopx-/-) was generated. We then studied the biological effects of Hopx knockout on the hematopoietic system of young mice, via whole-transcriptome RNA-seq.

2023-02-18 | GSE145507 | GEO

Role of Hopx in myogenesis and commitment [HopxKO]

Project description:Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Hopx labels cardiac progenitors that are commited to the cardiac myocyte lineage. Hopx-deficiency leads to thin myocardium in approximately mid-gestation lethality in approximately 50% of embryos (secondary to thin myocardium and presumed cardiac rupture). Hopx-/- EBs display impaired myogenesis during cardiac differentiation. ChIP-seq and RNA expression analysis suggests that Hopx down regulates Wnt signaling by directly occupying and repressing wnt ligand genes. Analysis of embryoid bodies on day 8 of cardiac differentiation. RNA was made of from 1. Hopx +/- embryoid bodies, 2. Hopx -/- embryoid bodies, Embryonic stem cell lines were derived from littermate mouse blastocysts. Results provide insight into gene programs regulated by Hopx in cardiac development.

2015-06-01 | GSE67253 | GEO

Dlx3 Regulates Lifr and Chrdl1 Expression in Mouse Embryonic Stem Cell Differentiation

Project description:Dlx3 over-expression in mouse embryonic fibroblasts changed the expression level of numerous genes involved in osteogenesis and embryonic stem cell-related pathways as revealed by microarray analysis. From the list of Dlx3 modulated genes we focused our attention on the study of two candidates, Lifr and Chrdl1. Chromatin immunoprecipitation demonstrated the recruitment of Dlx3 transcription factor to the promoters of Lifr and Chrdl1, and luciferase assays confirmed the role of Dlx3 in the regulation of Lifr expression. Over-expression of Dlx3 in mouse embryonic stem cells stimulated Lifr and Chrdl1 expression and inhibited expression of Id proteins and Bmp4. We show that Dlx3 increases the expression of both soluble and transmembrane forms of Lifr. Soluble Lifr may regulate extracellular Lif levels via solution binding, while transmembrane Lifr mediates the signal transduction pathway. The data suggests that Dlx3 may be involved in stem cell differentiation in a dosage dependent way through its interaction with Lifr and with Chrdl1, a known antagonist of Bmp4. We speculate that Dlx3 may also be involved in osteoblast differentiation through interactions involving Lifr, Bmp, and Id proteins and signaling via the JAK/STAT and MAPK pathways. In summary, our data suggests that Dlx3 proteins play a significant role in a highly tuned network in early embryogenesis. Keywords: treated vs.untreated Stable and Transient transfection of Dlx3 in MEF. Total of 4 hybridizations including biological replicates.

2009-08-15 | E-GEOD-11727 | biostudies-arrayexpress

Gene expression profiling: human CD8+CD45RO+ memory T cells in IL23 responsive and nonresponsive individuals

Project description:The interleukin-23 (IL-23) pathway plays a critical role in the pathogenesis of multiple chronic inflammatory disorders, however, inter-individual variability in IL-23-induced signal transduction in circulating human lymphocytes has not been well-defined. In this study, we observed marked, reproducible inter-individual differences in IL-23 responsiveness (measured by STAT3 phosphorylation) in peripheral blood CD8+CD45RO+ memory T and CD3+CD56+ NKT cells. To define mechanisms that might be contributing to the differential IL-23-induced STAT3 activation between individuals, we examined mRNA expression differences in CD8+CD45RO+ memory T cells between IL-23 responsive and non-responsive individuals. We analyzed unstimulated and IL-23 stimulated FACS sorted CD8+CD45RO+ memory T cells from two individuals demonstrating robust IL-23 responsiveness, and two individuals demonstrating low IL-23 responsiveness, using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Affymetrix Expression Console software. No techinical replicates were performed.

2013-03-08 | E-GEOD-42051 | biostudies-arrayexpress

Role of Hopx in myogenesis and commitment [HopxKO+Wnt]

Project description:Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Hopx labels cardiac progenitors that are commited to the cardiac myocyte lineage. Hopx-deficiency leads to thin myocardium in approximately mid-gestation lethality in approximately 50% of embryos (secondary to thin myocardium and presumed cardiac rupture). Hopx-/- EBs display impaired myogenesis during cardiac differentiation. ChIP-seq and RNA expression analysis suggests that Hopx down regulates Wnt signaling by directly occupying and repressing wnt ligand genes. Analysis of embryoid bodies on day 8 of cardiac differentiation. RNA was made of from Hopx +/- embryoid bodies or Hopx -/- embryoid bodies treated with 12.5 uM XAV939. Heterozygous embryoid bodies included 0 uM XAV939, a well-characterized, known Wnt inhibitor. Embryonic stem cell lines were derived from littermate mouse blastocysts. Results provide insight into gene programs regulated by Hopx in cardiac development.

2015-06-01 | GSE67252 | GEO

Competitive regulation of HOPX transcription governs cardiomyocyte maturation

Project description:This study establishes the homeodomain only protein, HOPX, as a determinant controlling the molecular switch between cardiomyocyte progenitor and maturation gene programs. This dataset is about time-course CAGE (capped analysis of gene expression) data with genome-wide active transcription footprinting. HOPX CRISPRi cells were differentiated into cardiomyocytes ± DOX and analyzed by CAGE sequencing, among other methods. The study revealed that HOPX interacts with and controls core cardiac networks by regulating the activity of mutually exclusive developmental gene programs.

2022-05-21 | E-MTAB-11719 | biostudies-arrayexpress

Role of Hopx in myogenesis and commitment [ChIP-Seq]

Project description:Hopx is expressed in cardiomyoblasts, progenitors commited to the myocyte fate. ChIP-seq experiements were performed to understand Hopx occupancy in E9.5 hearts. An epitope tagged allele, in which a 3X-Flag sequence is appeneded to the endogenous Hopx transcript. Our results suggest that Hopx occupancy is enriched in regions close to Wnt family members, confirmed by gene ontology analysis and indepedent expression analysis.

2015-06-01 | GSE67251 | GEO

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