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accession-icon SRP124495
Neonatally imprinted mesenteric lymph node stromal cell subsets induce tolerogenic dendritic cells [Tx FSC]
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gut-draining mesenteric lymph nodes (mLNs) play a key role in peripheral tolerance towards food and commensal antigens by providing an optimal microenvironment for efficient de novo induction of Foxp3+ regulatory T cells (Tregs). We recently identified mLN stromal cells as critical cellular players in this process and demonstrated that their tolerogenic properties are imprinted by microbiota. Here, we show that this imprinting process already takes place in the neonatal phase and renders the mLN stromal cell compartment resistant to inflammatory perturbations later in life. Utilizing LN transplantation, RNA-seq and single-cell RNA-seq allowed identification of stably imprinted expression signatures in mLN fibroblastic stromal cells. We dissected common stromal cell subsets across gut-draining mLNs and skin-draining LNs with location-specific immunomodulatory functions, such as subset-specific expression of Aldh1a2/3. Accordingly, mLN stromal cells shaped resident dendritic cells to attain high Treg-inducing capacity in a Bmp2-dependent manner. Thus, crosstalk between mLN stromal and resident dendritic cells provides a robust feedback mechanism for the maintenance of intestinal tolerance. Overall design: Transcriptomic analysis of fibroblastic stromal cells of skin-draining and intestinal-draining lymph nodes from endogenous and transplanted lymph nodes at the popliteal fossa.

Publication Title

Neonatally imprinted stromal cell subsets induce tolerogenic dendritic cells in mesenteric lymph nodes.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP124959
Neonatally imprinted mesenteric lymph node stromal cell subsets induce tolerogenic dendritic cells [resDCs]
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gut-draining mesenteric lymph nodes (mLNs) play a key role in peripheral tolerance towards food and commensal antigens by providing an optimal microenvironment for efficient de novo induction of Foxp3+ regulatory T cells (Tregs). We recently identified mLN stromal cells as critical cellular players in this process and demonstrated that their tolerogenic properties are imprinted by microbiota. Here, we show that this imprinting process already takes place in the neonatal phase and renders the mLN stromal cell compartment resistant to inflammatory perturbations later in life. Utilizing LN transplantation, RNA-seq and single-cell RNA-seq allowed identification of stably imprinted expression signatures in mLN fibroblastic stromal cells. We dissected common stromal cell subsets across gut-draining mLNs and skin-draining LNs with location-specific immunomodulatory functions, such as subset-specific expression of Aldh1a2/3. Accordingly, mLN stromal cells shaped resident dendritic cells to attain high Treg-inducing capacity in a Bmp2-dependent manner. Thus, crosstalk between mLN stromal and resident dendritic cells provides a robust feedback mechanism for the maintenance of intestinal tolerance. Overall design: Transcriptomic analysis of resident dendritic cells of skin-draining and intestinal-draining lymph nodes from endogenous and lymph nodes transplanted to the popliteal fossa.

Publication Title

Neonatally imprinted stromal cell subsets induce tolerogenic dendritic cells in mesenteric lymph nodes.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP150769
Neonatally imprinted mesenteric lymph node stromal cell subsets induce tolerogenic dendritic cells [migDC]
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gut-draining mesenteric lymph nodes (mLNs) play a key role in peripheral tolerance towards food and commensal antigens by providing an optimal microenvironment for efficient de novo induction of Foxp3+ regulatory T cells (Tregs). We recently identified mLN stromal cells as critical cellular players in this process and demonstrated that their tolerogenic properties are imprinted by microbiota. Here, we show that this imprinting process already takes place in the neonatal phase and renders the mLN stromal cell compartment resistant to inflammatory perturbations later in life. Utilizing LN transplantation, RNA-seq and single-cell RNA-seq allowed identification of stably imprinted expression signatures in mLN fibroblastic stromal cells. We dissected common stromal cell subsets across gut-draining mLNs and skin-draining LNs with location-specific immunomodulatory functions, such as subset-specific expression of Aldh1a2/3. Accordingly, mLN stromal cells shaped resident dendritic cells to attain high Treg-inducing capacity in a Bmp2-dependent manner. Thus, crosstalk between mLN stromal and resident dendritic cells provides a robust feedback mechanism for the maintenance of intestinal tolerance. Overall design: Transcriptomic analysis of migratory dendritic cells of skin-draining and intestinal-draining lymph nodes from endogenous and lymph nodes transplanted to the popliteal fossa.

Publication Title

Neonatally imprinted stromal cell subsets induce tolerogenic dendritic cells in mesenteric lymph nodes.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE110085
Comparison of primary vs immortalized HUVEC
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Fundamental research and drug development for personalized medicine necessitates cell cultures from defined genetic backgrounds. However, providing sufficient numbers of authentic cells from individuals poses a challenge. Here, we present a new strategy for rapid cell expansion that overcomes current limitations. Using a small gene library, we expanded primary cells from different tissues, donors and species. Cell type specific regimens that allow the reproducible creation of cell lines were identified. In depth characterization of a series of endothelial and hepatocytic cell lines confirmed phenotypic stability and functionality. Applying this technology enables rapid, efficient and reliable production of unlimited numbers of personalized cells. As such, these cell systems support mechanistic studies, epidemiological research and tailored drug development.

Publication Title

Expansion of functional personalized cells with specific transgene combinations.

Sample Metadata Fields

Specimen part

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accession-icon GSE10580
Genes regulated by PRDM5 in U2OS cells.
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

PRDM5 is a recently identified member of the PRDM family of proteins, which functions as a transcriptional repressor by recruiting histone methyltransferase G9A to DNA, and behaves as a putative tumor suppressor in different types of cancer.

Publication Title

The tumor suppressor PRDM5 regulates Wnt signaling at early stages of zebrafish development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14204
25-hydroxycholesterol effects on human hepatocyte metabolism and the antiviral state it conveys against the HCV
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Hepatitis C virus (HCV) infection is a global health problem. A number of studies have implicated a direct role of cellular lipid metabolism in the HCV life cycle and inhibitors of the mevalonate pathway have been demonstrated to result in an antiviral state within the host cell. Transcriptome profiling was also conducted on Huh-7 human hepatoma cells bearing subgenomic HCV replicons with and without treatment with 25-hydroxycholesterol (25-HC), an inhibitor of the mevalonate pathway that alters lipid metabolism, to assess metabolic determinants of pro- and antiviral states within the host cell.

Publication Title

Transcriptional profiling of the effects of 25-hydroxycholesterol on human hepatocyte metabolism and the antiviral state it conveys against the hepatitis C virus.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP049391
Next-Generation Sequencing Analysis Reveals Differential Expression Profiles of miRNA-mRNA Target Pairs in KSHV-Infected Cells [mRNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

This SuperSeries is composed of the SubSeries listed below. Purpose: Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) causes several lymphoproliferative disorders, including KS, a common AIDS-associated malignancy. Cellular and viral microRNAs (miRNAs) have been shown to play important roles in regulating the expression of genes in oncogenesis. Herpesviruses, including KSHV, encode for miRNAs that are involved in angiogenesis, inflammation and apoptosis. A better knowledge of the miRNA-mediated pathways that regulate KSHV infection is therefore essential for an improved understanding of viral infection and pathogenesis. Methods: In this study, we used deep sequencing to analyze miRNA, both viral and human, and mRNA expression in KS tumor-derived human cells. Results: This approach revealed 153 differentially expressed human miRNAs between KSHV-positive and -negative cells. Differential expression of eight miRNAs was independently confirmed by qRT-PCR. We additionally showed that a majority (~73%) of KSHV-regulated miRNAs are down-regulated, including most members of the 14q32 miRNA cluster. Specifically, human miR-409-3p, which is known to target the pro-angiogenic growth factor angiogenin and the inflammation marker fibrinogen-beta, was significantly down-regulated in KSHV-infected cells based on deep sequencing and qRT-PCR. Despite this substantial down-regulation of cellular miRNAs, hsa-miR-708-5p was significantly up-regulated by KSHV and has been shown to directly inhibit pro-apoptotic protease Caspase-2. Finally, we evaluated to what extent there was an inverse correlation between miRNA and mRNA expression levels. Using filtered datasets, we identified relevant canonical pathways that were significantly enriched. Conclusion: Taken together, our data demonstrate that most human miRNAs affected by KSHV are repressed and our findings highlight the relevance of studying the post-transcriptional gene regulation of miRNAs for KSHV-associated malignancies. Overall design: Refer to individual Series. 6 samples analyzed (one cell type). Two experimental conditions: uninfected vs. chronically KSHV-infected cells (n=3). Two sequencing platforms: microRNA-Seq and mRNA-Seq.

Publication Title

Next-Generation Sequencing Analysis Reveals Differential Expression Profiles of MiRNA-mRNA Target Pairs in KSHV-Infected Cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14889
A caspase-independent necrotic death is activated by isopeptidase inhibitor G5 in apoptosis-resistant glioblastoma cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The regulation of necrotic death and its relevance in anti-cancer therapy are largely unknown. Here we have investigated the pro-apoptotic and pro-necrotic activities of two ubiquitin-proteasome system inhibitors (UPSIs): bortezomib and G5. The present study points out that the glioblastoma cell lines U87MG and T98G are useful models to study the susceptibility to apoptosis and necrosis in response to UPSIs. U87MG cells are resistant to apoptosis induced by bortezomib and G5 but susceptible to necrosis induced by G5. On the opposite T98G cells are susceptible to apoptosis induced by both inhibitors but show some resistance to G5-induced necrosis. By comparing the transcriptional profiles of the two cell lines, we have found that the resistance to G5-induced necrosis could arise from differences in glutathione synthesis/utilization and in the microenvironment. In particular collagen IV, which is highly expressed in T98G cells, and fibronectin, whose adhesive function is counteracted by tenascin-C in U87MG cells, can restrain the necrotic response to G5. Collectively, our results provide an initial characterization of the molecular signals governing cell death by necrosis in glioblastoma cell lines.

Publication Title

Characterization of caspase-dependent and caspase-independent deaths in glioblastoma cells treated with inhibitors of the ubiquitin-proteasome system.

Sample Metadata Fields

Cell line

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accession-icon GSE139027
Transcriptomics analysis of cells transfected with miR-183 cluster mimics and immunostimulated with poly(I:C)
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Our work demonstrated that miR-183 cluster regulates IFN production and signaling

Publication Title

A conserved miRNA-183 cluster regulates the innate antiviral response.

Sample Metadata Fields

Cell line

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accession-icon GSE56583
Effects of vitamin D supplementation on alveolar macrophage gene expression
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

The objective of the overall study was to determine the effects of oral vitamin D supplementation on alveolar macrophages from human subjects. In this substudy, subjects treated with vitamin D (intervention group) in paired analysis had small, but significant effects on immune-related differential gene expression pre versus post supplementation.

Publication Title

Effects of vitamin D supplementation on alveolar macrophage gene expression: preliminary results of a randomized, controlled trial.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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