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accession-icon GSE74854
Id2 is required for antiviral Th1 cell differentiation and represses Tfh cell differentiation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Differentiation of naive CD4+ T cells into T-helper (Th) effector subsets is critical for protection against pathogens. Together, E-protein transcription factors and the inhibitor-of-DNA binding (Id) proteins are important arbiters of T cell development, but their role in the differentiation of Th1 and Tfh cells is not well understood. Th1 cells show robust Id2 expression compared to Tfh cells, and RNAi depletion of Id2 increased Tfh cell frequencies and germinal center responses, while impairing Th1 cell accumulation during viral infection. Further, Th1 cell differentiation was blocked by genetic ablation of Id2, leading to E-protein dependent accumulation of effector cells with 78% of Th1-associated genes showing diminished expression and a concurrent enrichment of the Tfh gene-expression program. The Tfh-defining transcriptional repressor Bcl6 bound to the Id2 locus inhibiting expression, providing a mechanism by which bimodal expression of Id2 in Tfh and Th1 cells can be established. Thus, Id2 is critical in enforcing the reciprocal development of Th1 and Tfh cell fates.

Publication Title

Id2 reinforces TH1 differentiation and inhibits E2A to repress TFH differentiation.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE2331
Rat mammary expression in individuals and pools
  • organism-icon Rattus norvegicus
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

Rat mammary glands were obtained from individual rats in RXR treated (a) and control (b) conditions (12 rats in each condition). The 24 samples were hybridized individually. Also, in each condition, samples were combined into different pools of 2, pools of 3, pools of 12. Technical replicates were also run.

Publication Title

On the utility of pooling biological samples in microarray experiments.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42938
Abrupt scrib- vs. Abrupt and RasV12 (RasACT) scrib-, NotchICD (NACT) scrib- +/- JNK (Bsk) expression profiles
  • organism-icon Drosophila melanogaster
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Drosophila mosaic eye-antennal discs from the listed genotypes generated using the MARCM system were dissected from 3rd instar larvae at day 5 after egg deposition.

Publication Title

The BTB-zinc finger transcription factor abrupt acts as an epithelial oncogene in Drosophila melanogaster through maintaining a progenitor-like cell state.

Sample Metadata Fields

Specimen part

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accession-icon GSE21016
Genome-wide analysis of gene expression profiles in ITNK
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of gene expression profiles in Induced T-to-Natural Killer (ITNK), compared to DN3 parental T cells and IL-2-expanded NK cells (LAK). The hypothesis tested in the present study was that gene expression profiles of ITNK that were derived from DN3 T cells after deletion of Bcl11b were more similar to LAK, rather than DN3 T cells. Results provide important information of the ITNKs, such as canditate genes regulated by Bcl11b, up-regulated important genes expressed in NK cells, and down-regulated T cell genes.

Publication Title

Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion.

Sample Metadata Fields

Specimen part

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accession-icon SRP042158
RNA-seq analysis of vorinostat-resistant HCT116 cells following gene knockdown of GLI1 or PSMD13 with or without vorinostat treatment
  • organism-icon Homo sapiens
  • sample-icon 42 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Transcriptome analysis was conducted on vorinostat resistant HCT116 cells (HCT116-VR) upon knockdown of potential vorinostat resistance candidate genes in the presence and absence of vorinostat. Potential vorinostat resistance candidate genes chosen for this study were GLI1 and PSMD13, which were identified through a genome-wide synthetic lethal RNA interference screen. To understand the transcriptional events underpinning the effect of GLI1 and PSMD13 knockdown (sensitisation to vorinostat-induced apoptosis), cells were first subjected to gene knockdown, then to treatment with vorinsotat or the solvent control. Two timepoints for drug treatment were assessed: a timepoint before induction of apoptosis (4hrs for siGLI1 and 8hrs for siPSMD13) and a timepoint when apoptosis could be detected (8hrs for siGLI1 and 12hrs for siPSMD13). Overall design: There are 42 samples in total, from triplicate independent biological experiments of 14 samples each.

Publication Title

A genome scale RNAi screen identifies GLI1 as a novel gene regulating vorinostat sensitivity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15192
Differences between CD44+/CD24- and CD44-/CD24+ subpopulation of immortalized human mammary epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

CD44+/CD24- subpopulation of normal and cancerous breast epithelial cells are suggested to have stem cell properties. The goal of this study was to identify gene expression differences between CD44+/CD24- and CD44-/CD24+ subpopulation of cells from a same cell lines. We selected MCF-10A cells, which are immortalized derived from a fibrocystic breast disease. These cells are immortalized but not transformed and express basal cell markers.

Publication Title

SLUG/SNAI2 and tumor necrosis factor generate breast cells with CD44+/CD24- phenotype.

Sample Metadata Fields

Specimen part

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accession-icon SRP080852
T cell oxygen-sensing proteins establish an immunologically tolerant metastatic niche
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 2500

Description

Cancer cells must evade immune responses at distant sites to establish metastases. The lung is a frequent site for metastasis. We hypothesized that lung-specific immunoregulatory mechanisms create an immunologically permissive environment for tumor colonization. We found that T cell-intrinsic expression of the oxygen-sensing prolyl-hydroxylase (PHD) proteins is required to maintain local tolerance against innocuous antigens in the lung, but powerfully licenses colonization by circulating tumor cells. PHD proteins limit pulmonary type helper (Th)-1 responses, promote CD4+-regulatory T (Treg) cell induction, and restrain CD8+ T cell effector function. Tumor colonization is accompanied by PHD protein-dependent induction of pulmonary Treg cells and suppression of IFN-g-dependent tumor clearance. T cell-intrinsic deletion or pharmacological inhibition of PHD proteins limits tumor colonization of the lung and improves the efficacy of adoptive cell transfer immunotherapy. Collectively, PHD proteins function in T cells to coordinate distinct immunoregulatory programs within the lung that are permissive to cancer metastasis. Overall design: RNA expression was measured by RNA-Seq at day 4 following stimulation of naïve FACS-sorted CD4+ T cells with anti-CD3 and anti-CD28 antibodies in the presence of indicated doses of TGF-b. Gene expression was analysed separately in control Cd4Cre (WT) and Egln1fl/fl Egln2fl/fl Egln3fl/fl Cd4Cre (tKO) cells, or in cells treated with the pharmacological PHD inhibitor dimethyloxaloylglycine (DMOG) and control vehicle-treated cells.

Publication Title

Oxygen Sensing by T Cells Establishes an Immunologically Tolerant Metastatic Niche.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE72752
CD39 expression identifies terminally exhausted CD8+ T cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Exhausted T cells express multiple co-inhibitory molecules that impair their function and limit immunity to chronic viral infection. Defining novel markers of exhaustion is important both for identifying and potentially reversing T cell exhaustion. Herein, we show that the ectonucleotidse CD39 is a marker of exhausted CD8+ T cells. CD8+ T cells specific for HCV or HIV express high levels of CD39, but those specific for EBV and CMV do not. CD39 expressed by CD8+ T cells in chronic infection is enzymatically active, co-expressed with PD-1, marks cells with a transcriptional signature of T cell exhaustion and correlates with viral load in HIV and HCV. In the mouse model of chronic Lymphocytic Choriomeningitis Virus infection, virus-specific CD8+ T cells contain a population of CD39high CD8+ T cells that is absent in functional memory cells elicited by acute infection. This CD39high CD8+ T cell population is enriched for cells with the phenotypic and functional profile of terminal exhaustion. These findings provide a new marker of T cell exhaustion, and implicate the purinergic pathway in the regulation of T cell exhaustion.

Publication Title

CD39 Expression Identifies Terminally Exhausted CD8+ T Cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP112535
Profiling of untreated and residual murine BCC after Hedgehog Pathway Inhibitor
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNA was isolated from laser capture micro-dissected (LCM) tumour nests from fresh frozen skin of K14Cre-ER; Ptch1fl/fl; p53fl/fl mice either before (untreated) or after (treated) 28 days of twice a day vismodegib dosing at 75mg/kg body weight by oral gavage. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0014355 Overall design: Gene expression profiling of tumour cells from BCC mice before and after 28 days of vismodegib treatment

Publication Title

A cell identity switch allows residual BCC to survive Hedgehog pathway inhibition.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE111474
Distinct constitutive and pathogen-induced transcriptional programs in dendritic cells derived from CD16- versus CD16+ monocytes
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Classical CD16- versus intermediate/non-classical CD16+ monocytes differ in their homing potential and immunological functions; but whether they differentiate into dendritic cells (DC) with distinct contributions to immunity against bacterial/viral pathogens remains poorly investigated. Here, we employed a systems biology approach to identify differences between CD16+ and CD16- monocyte-derived DC (MDDC) with potential clinical relevance

Publication Title

CD16<sup>+</sup> monocytes give rise to CD103<sup>+</sup>RALDH2<sup>+</sup>TCF4<sup>+</sup> dendritic cells with unique transcriptional and immunological features.

Sample Metadata Fields

Subject

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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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