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accession-icon GSE63662
GM-CSF induced gene-regulation in human monocytes
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human and murine studies showed that granulocyte macrophage colony-stimulating factor (GM-CSF) exerts beneficial effects in intestinal inflammation. To explore whether GM-CSF mediates its effects via monocytes, we analyzed effects of GM-CSF on monocytes in vitro and assessed the immunomodulatory potential of GM-CSF-activated monocytes (GMaM). We used microarray technology and functional assays to characterize GMaM in vitro and used a mouse model of colitis to study GMaM functions in vivo.

Publication Title

Reprogramming of monocytes by GM-CSF contributes to regulatory immune functions during intestinal inflammation.

Sample Metadata Fields

Specimen part

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accession-icon GSE54980
Sulforaphane protects from T cell mediated autoimmune disease by inhibition of interleukin 23 and 12 in dendritic cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Sulforaphane (SFN), an isothiocyanate, is part of an important group of naturally occurring small molecules with antiinflammatory properties. Even though the published reports are vague, most are best conceivable with an inhibition of T cell functions. We therefore analyzed the effect of SFN on T cell-mediated autoimmune disease. Feeding mice with SFN protected from severe experimental autoimmune encephalomyelitis (EAE). Disease amelioration was associated with reduced interleukin (IL)-17 and IFN-gamma expression in draining lymph nodes. In vitro, SFN treatment of T cells did not directly alter T cell cytokine secretion. In contrast, SFN treatment of dendritic cells (DC) inhibited TLR4-induced IL-12 and IL-23 production and the cytokine profile of T cells stimulated by SFN-treated DC. SFN suppressed TLR4-induced nuclear factor kappa B (NFB) activity, without affecting the degradation of its inhibitor (IB). Instead, SFN treatment of DC resulted in strong expression of the stress response protein heme oxygenase-1 (HO-1), which interacts with NFB p65 and inhibits its activity. Consistent with these findings, HO-1 bound to p65 and subsequently inhibited the p65 promoter activity within the IL23a and IL12b promoter region. Importantly, SFN suppressed Il23a and Il12b expression in vivo and silenced Th17/Th1 responses within the CNS . Our data show that SFN improves Th17/Th1-mediated autoimmune disease by inducing HO-1 and inhibiting p65-regulated IL-23 and IL-12 expression.

Publication Title

Sulforaphane protects from T cell-mediated autoimmune disease by inhibition of IL-23 and IL-12 in dendritic cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP045900
Next Generation Sequencing of Pattern II Demyelinating Brain Lesions from a Multiple Sclerosis Patient
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system with marked heterogeneity in several aspects including pathological processes. Four histopathological patterns of MS have been described. Pattern II is characterized by infiltrating macrophages and T-cells and by antibody and complement deposition. Transcriptome analysis of three patern II demyelinating brain lesions from a multiple sclerosis patient using RNA sequencing demonstrated the presence of mRNA transcripts for genes specific of activated macrophages, T and B cells as well as genes coding for immunoglobulins, complement proteins and some pattern II associated proteins, providing additional evidence supporting pattern II demyelination. Overall design: Examination of 3 different demyelinating lesions identified by Immunohistopathology.

Publication Title

Central role of Th2/Tc2 lymphocytes in pattern II multiple sclerosis lesions.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP096989
Next Generation Sequencing of splenic- and CNS-infiltrating OT-1 cells in ODC-OVA mice upon LCMV-OVA and Lm-OVA infection
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goal of this study is to compare the transcriptome of OT-1 cells during priming (3 days after infection) and during effector phase ( 7 days after infection) in ODC-OVA mice after LCMV-OVA and Lm-OVA infection Overall design: OT-1 mRNA profiles of 7-weeks old ODC-OVA mice adoptively transfered with 10^5 OT-1 CD45.1 cells 3 and 7 days after i.v. infection with LCMV-OVA and Lm-OVA (deep sequencing, in triplicate, using Illumina).

Publication Title

Expression of the DNA-Binding Factor TOX Promotes the Encephalitogenic Potential of Microbe-Induced Autoreactive CD8<sup>+</sup> T Cells.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP096988
Next Generation Sequencing of CNS-infiltrating Tox-sufficient and -deficient OT-1 cells in ODC-OVA mice 7 days after LCMV-OVA infection
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goal of this study is to compare the transcriptome of CNS-infiltrating OT-1 WT and Tox-deficient cells during effector phase (7 days after infection with LCMV-OVA) Overall design: OT-1 mRNA profiles of 7-weeks old ODC-OVA mice adoptively transfered with 10^5 OT-1 CD45.1 cells (WT and Tox-deficient) 7 days after i.v. infection with LCMV-OVA (deep sequencing, in triplicate, using Illumina).

Publication Title

Expression of the DNA-Binding Factor TOX Promotes the Encephalitogenic Potential of Microbe-Induced Autoreactive CD8<sup>+</sup> T Cells.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP165279
Early response to loss of Argonaute proteins in embryonic stem cells activates the Tgf-ß/Smad Transcriptional Network [mRNA-Seq: DicerDgcr8_KOs]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Argonaute (Ago) proteins, which act in post-transcriptional gene regulation directed by small RNAs, are vital for normal stem cell biology. Here we report the genomic characterization of stable Ago-deficient mouse embryonic stem cells (mESC) and determine the direct, primary and system level response to loss of Ago-mediated regulation. We find mESCs lacking all four Ago proteins are viable, do not repress microRNA (miRNA)-targeted cellular RNAs, and show distinctive gene network signatures. Profiling of RNA expression and epigenetic activity in an Ago mutant genetic series indicates that early responses to Ago loss are driven by transcriptional regulatory networks, in particular the Tgf-ß/Smad transcriptional network. This finding is confirmed using a time course analysis of Ago depletion and Ago rescue experiments. Detailed analysis places Tgf-ß/Smad activation upstream of cell cycle regulator activation, such as Cdkn1a, and repression of the c-Myc transcriptional network. The Tgf-ß/Smad pathway is directly controlled by multiple low-affinity miRNA interactions with Tgf-ß/Activin receptor mRNAs and receptor-mediated activation is required for Tgf-ß/Smad target induction with Ago loss. Our characterization reveals the interplay of post-transcriptional regulatory pathways with transcriptional networks in maintaining cell state and likely coordinating cell state transitions. Overall design: mRNA seq from stable genetic Dicer and Dgcr8 mutant mouse embryonic stem cells.

Publication Title

Temporal Control of the TGF-β Signaling Network by Mouse ESC MicroRNA Targets of Different Affinities.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE107333
Endogenous retrovirus-associated genes in a hypoxia-mimetic cobalt chloride neuroblastoma model
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

By using high-density DNA microarrays, we analyzed the gene-expression profile of SHSY5Y neuroblastoma cells after treatment with cobalt chloride

Publication Title

Investigation of Endogenous Retrovirus Sequences in the Neighborhood of Genes Up-regulated in a Neuroblastoma Model after Treatment with Hypoxia-Mimetic Cobalt Chloride.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE56989
Genome-wide identification of HIF-1 and HIF-2 binding sites in hypoxic human macrophages alternatively activated by IL-10
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Primary human macrophages with a HIF-1alpha or HIF-2alpha knockdown were pretreated with IL-10 for 16h and afterwards for 4h additionaly under hypoxi (1% O2), RNA was isolated usind the Qiagen RNAeasy Kit and cDNA synthesis wos done using Ambion WT Expression Kit. Expression was compared to si control under control conditions.

Publication Title

Genome-wide identification of hypoxia-inducible factor-1 and -2 binding sites in hypoxic human macrophages alternatively activated by IL-10.

Sample Metadata Fields

Specimen part

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accession-icon GSE30143
Gene expression profiling in lungs of mice with mesenchyme-specific GR ablation (GRCol1-Cre)
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

The goal of the experiment was to assay the role of the glucocorticoid receptor (GR) in development of mesenchynmal cells of the lung occuring between the 16 and 18 day of embryonal development.

Publication Title

Glucocorticoid activity during lung maturation is essential in mesenchymal and less in alveolar epithelial cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE47065
Gene expression profiling of IR-/-, IGF-1R-/- (dKO) newborn epidermis.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Analysis of newborn mouse epidermis lacking the expression of Insulin receptor (IR) and Insulin like growth factor 1 receptor (IGF-1R). Results show that IR/IGF-1R signalling control epidermal morphogenesis.

Publication Title

Insulin/IGF-1 controls epidermal morphogenesis via regulation of FoxO-mediated p63 inhibition.

Sample Metadata Fields

No sample metadata fields

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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