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accession-icon GSE50400
Suppression of molecular inflammatory pathways by Toll-like Receptor 7, 8, and 9 antagonists in a model of IL-23-induced skin inflammation
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

Psoriasis is a complex inflammatory disease resulting from the activation of T helper (Th) 1 and Th17 cells. Recent evidence suggests that abnormal activation of Toll-like receptors (TLRs) 7, 8 and 9 contributes to the initiation and maintenance of psoriasis. We have evaluated the effects of TLR antagonists on the gene expression profile in an IL-23-induced skin inflammation model in mice. Psoriasis-like skin lesions were induced in C57BL/6 mice by intradermal injection of IL-23 in the dorsum. Two TLR antagonists were compared: IMO-3100, an antagonist of TLRs 7 and 9, and IMO-8400, an antagonist of TLRs 7, 8 and 9, both of which previously have been shown to reduce epidermal hyperplasia in this model. Skin gene expression profiles of IL-23-induced inflammation were compared with or without TLR antagonist treatment. IL-23 injection resulted in alteration of 5100 gene probes (fold change 2, FDR < 0.05) including IL-17 pathways that are up-regulated in psoriasis vulgaris. Targeting TLRs 7, 8 and 9 with IMO-8400 resulted in modulation of more than 2300 mRNAs while targeting TLRs 7 and 9 with IMO-3100 resulted in modulation of more than 1900 mRNAs. Both agents strongly decreased IL-17A expression (>12-fold reduction), normalized IL-17 induced genes such as beta-defensin and CXCL1, and normalized aberrant expression of keratin 16 (indicating epidermal hyperplasia). These results suggest that IL-23-driven inflammation in mouse skin may be dependent on signaling mediated by TLRs 7, 8, and 9 and that these receptors represent novel therapeutic targets in psoriasis vulgaris and other diseases with similar pathophysiology.

Publication Title

Suppression of molecular inflammatory pathways by Toll-like receptor 7, 8, and 9 antagonists in a model of IL-23-induced skin inflammation.

Sample Metadata Fields

Treatment

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accession-icon GSE17989
Influence of T and B lymphocytes on the antigen presentation capacities of splenic conventional dendritic cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

The goal of this project was to characterize DCs from lymphopenic mice, like RAG (recombination activated gene) deficient mice and to examine the influence of mature B and T cells on the antigen presenting ability of splenic cDCs. We demonstrate how cellular cross-talk can shape the character and function of cDCs. Lymphopenic conditions, where splenic cDCs have to develop and differentiate, drastically change their character and their ability to cross-present soluble antigen.

Publication Title

Immunoglobulins drive terminal maturation of splenic dendritic cells.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE108640
Ichthyosis molecular fingerprinting shows profound Th17-skewing and a unique barrier genomic signature
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The purpose of this study was to analyze the genomic signatures and profiles of skin from ichthyosis (various subtypes) vs. healthy patients. The analysis strategy was to study differentially expressed genes common to the ichthyosis shared phenotype, as well as individual ichthyosis subtypes, and compare and contrast to the genomic profiles of atopic dermatitis and psoriasis.

Publication Title

Ichthyosis molecular fingerprinting shows profound T&lt;sub&gt;H&lt;/sub&gt;17 skewing and a unique barrier genomic signature.

Sample Metadata Fields

Age, Specimen part, Disease

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accession-icon GSE19002
Microarray analysis of defective cartilage in Hoxc8- and Hoxd4-transgenic mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE18992
Overexpression of Hoxc8 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxc8 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.

Publication Title

Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE18991
Overexpression of Hoxd4 transcription factor alters transcriptional profiles in mouse chondrocytes at E18.5
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxd4 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.

Publication Title

Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE30268
Dynamic transcriptional events in embryonic stem cells mediated by the super elongation complex (SEC).
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Dynamic transcriptional events in embryonic stem cells mediated by the super elongation complex (SEC).

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE30176
Retinoic acid (RA) induction time-course to profile gene expression during mES cell differentiation.
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

Murine ES cell gene expression before RA induction are used to compare gene expression for time-points of 2, 4, 6hrs post-induction.

Publication Title

Dynamic transcriptional events in embryonic stem cells mediated by the super elongation complex (SEC).

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26037
Gene expression analysis in the absence of Creb in Pomc-expressing neurons of the hypothalamus
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

Brain-derived serotonin favors appetite in mice following its binding to the Htr1a and Htr2b receptors in arcuate neurons of the hypothalamus. In this study, we identified that CREB is the transcriptional effector of brain-derived serotonin control of appetite in arcuate nuclei.

Publication Title

Leptin-dependent serotonin control of appetite: temporal specificity, transcriptional regulation, and therapeutic implications.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE24451
Knockout of the Acyl CoA binding protein (ACBP) in mice - expression profile from the liver of 21 days old ACBP-/- and +/+ mice.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am

Publication Title

Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.

Sample Metadata Fields

Specimen part

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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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