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Homo sapiens
7 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Human peripheral blood monocytes (Mo) consist of subsets distinguished by expression of CD16 (FCGRIII) and chemokine receptors. Classical CD16- Mo express CCR2 and migrate in response to CCL2, while a minor CD16+ Mo subset expresses CX3CR1 and migrates into tissues expressing CX3CL1. CD16+ Mo produce pro-inflammatory cytokines and are expanded in certain inflammatory conditions including HIV infection.
Publication Title
Transcriptional profiling reveals developmental relationship and distinct biological functions of CD16+ and CD16- monocyte subsets.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- 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
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Huntington''s Disease (HD) is a fatal neurodegenerative disorder caused by an extended polyglutamine repeat in the N-terminus of the huntingtin (Htt) protein. Reactive microglia and elevated cytokine levels are observed in the brains of HD patients, but the extent to which neuroinflammation results from extrinsic or cell-autonomous mechanisms is unknown. Furthermore, the impact of microglia activation on the pathogenesis of HD remains to be established. Using genome-wide approaches, we show that expression of mutant Htt in microglia promotes cell-autonomous pro-inflammatory transcriptional activation within microglia by increasing the expression and transcriptional activities of the myeloid lineage-determining factors PU.1 and C/EBPs. Elevated levels of PU.1 and its target genes are observed in the brains of mouse models and HD individuals. Moreover, mutant Htt expressing microglia exhibit an increased capacity to induce neuronal death ex vivo and in vivo in the presence of sterile inflammation. These findings suggest that expression of mutant Htt in microglia may contribute to neuronal pathology in Huntingtin disease. Overall design: RNA-Seq and ChIP-Seq for PU.1, C/EBP, and H3K4me2 in BV2 cells and RNA-Seq in primary microglia and macrophages
Publication Title
Mutant Huntingtin promotes autonomous microglia activation via myeloid lineage-determining factors.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We previously demonstrated that Th1Th17 cells are highly permissive to HIV-1, whereas Th1 cells are relatively resistant. Here, we investigated molecular mechanisms underlying these differences. Superior HIV replication in Th1Th17 vs. Th1 cells was regulated by entry and post-entry mechanisms.
Publication Title
Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies peroxisome proliferator-activated receptor gamma as an intrinsic negative regulator of viral replication.
Sample Metadata Fields
Specimen part, Subject
View Samples- Saccharomyces cerevisiae
- 6 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
Experiments performed over the past three decades have shown that nucleosomes are transcriptional repressors. In Saccharomyces cerevisiae, depletion of histone H4 results in the genome-wide transcriptional de-repression of hundreds genes. The mechanism of de-repression is hypothesized to be rooted directly in chromatin changes. To test this, we reproduced classical H4 depletion experiments by conditional repression of all histone H3 transcription, which depletes the supply of nucleosomes in vivo. RNA-seq results were consistent with the earlier studies, but much more sensitive, revealing nearly 2500 de-repressed genes. Changes in chromatin organization were determined by MNase-seq. Nucleosomes that were preferentially retained occurred in regions of high DNA-encoded nucleosome affinity, and were marked with H3K36me2, which is linked to transcription elongation. Nucleosomes harboring acetyl marks or that contained the variant histone H2A.z were preferentially lost. Genes that were de-repressed lost or rearranged nucleosomes at their promoter, but not in the gene body. Therefore, a combination of DNA-encoded nucleosome stability and nucleosome composition dictates which nucleosomes will be lost under conditions of limiting histone protein. This, in turn, governs which genes will experience a loss of regulatory fidelity. Overall design: MNase-seq experiments consist of three wildtype (1 single-end and 2 paired-end) and four mutant (DCB200.1/H3 shutoff; 2 single-end, 2 paired-end) replicates. Each replicate contains two timepoints reflecting chromatin immediately after ("O hours") and 3 hours after transition to media containing dextrose. RNA-seq data includes three replicates from wildtype or H3 depleted cells after 3 hours in media containing dextrose.
Publication Title
In vivo effects of histone H3 depletion on nucleosome occupancy and position in Saccharomyces cerevisiae.
Sample Metadata Fields
Cell line, Subject, Time
View Samples- Homo sapiens
- 116 Downloadable Samples
Description
Langerhans cells (LC) represent one of the first lines of contact between the immune system and sexually transmitted pathogens, and in the human epidermis LCs have been thought to represent the only mononuclear phagocyte (MNP) population. Here we show an additional epidermal MNP subset that can be distinguished from LCs phenotypically as CD11chi, CD1c+ MR+ (epidermal CD11c+ DCs). These cells are transcriptionally similar to dermal cDC2 but express higher levels of costimulatory markers and are more efficient at T cell stimulation. Importantly, compared to LC, epidermal CD11c+ DCs are i) enriched in the epithelium of anogenital tissues where they preferentially interact with HIV, ii) express the higher levels of the HIV entry receptor CCR5, iii) support the higher levels of HIV uptake and replication and iv) are more efficient at transferring virus to CD4 T cells. Importantly these findings were observed using both a lab-adapted and transmitted/founder strain of HIV. We also describe a cell population that can be discerned from LCs by their lower surface expression of CD45, HLA-DR and CD33 (epidermal CD33low cells). These are transcriptionally similar to LCs but do not appear to function as APCs as do not secrete cytokines, express negligible amounts of costimulatory molecules and are very weak inducers of T cell proliferation. They also do not act as HIV target cells. Our findings reveal a new subset of epidermal DCs in skin and anogenital tissues with a potential key role in sexual transmission of HIV. Overall design: Sorted cell populations from four donors were captured directly into lysis buffer and polyA RNA transcripts were reverse transcribed, amplified and sequenced using the Smart-seq 2 protocol described by Picelli et al (Nature Methods. 2013;10(11):1096-8). Each sample was sequenced across 4 HiSeq lanes and the data for each lane is represented as an independent sample (GSM).
Publication Title
Identification of HIV transmitting CD11c<sup>+</sup> human epidermal dendritic cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 59 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.
Publication Title
Laboratory diet profoundly alters gene expression and confounds genomic analysis in mouse liver and lung.
Sample Metadata Fields
No sample metadata fields
View Samples
GSE11056- Mus musculus
- 55 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Exposure to high levels of arsenic in drinking water is associated with several types of cancers including lung, bladder and skin, as well as vascular disease and diabetes. Drinking water standards are based primarily on epidemiology and extrapolation from higher dose experiments, rather than measurements of phenotypic changes associated with chronic exposure to levels of arsenic similar to the current standard of 10ppb, and little is known about the difference between arsenic in food as opposed to arsenic in water. Measurement of phenotypic changes at low doses may be confounded by the effect of laboratory diet, in part because of trace amounts of arsenic in standard laboratory chows, but also because of broad metabolic changes in response to the chow itself. Finally, this series contrasts 8hr, 1mg/kg injected arsenic with the various chronic exposures, and also contrasts the acute effects of arsenic, dexamethasone or their combination. Male C57BL/6 mice were fed on two commercially available laboratory diets (LRD-5001 and AIN-76A) were chronically exposed, through drinking water or food, to environmentally relevant concentrations of sodium arsenite, or acutely exposed to dexamethasone.
Publication Title
Chronic exposure to arsenic in the drinking water alters the expression of immune response genes in mouse lung.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2500
Description
Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb or IFNg treatment in wild typ and Irf9-/- bone marrow derived macrophages. Overall design: Methods: Bone marrow derived macrophage mRNA of wild-type (WT) and Irf9 knock out mice (IRF9-/-) untreated, as well as 2h IFNb and IFNg treated were generated by deep sequencing, in triplicate, using Illumina sequencing.
Publication Title
A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2500
Description
Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb treatment in wild type and Irf9-/- mouse embryonic fibroblasts. Overall design: Methods: Mouse embryonic fibroblast (MEF) mRNA of wild-type (WT) and Irf9 knock out mice (IRF9-/-) untreated, as well as 2h IFNb treated were generated by deep sequencing, in triplicate, using Illumina sequencing.
Publication Title
A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.
Sample Metadata Fields
Subject
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