IFNα-induced gene expression in immortalized pig-tailed macaque CD4+ lymphocytes
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ABSTRACT:
PROVIDER: PRJNA522470 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8580540_1.fastq.gz | Fastqsanger.gz | |||
| SRR8580540_2.fastq.gz | Fastqsanger.gz | |||
| SRR8580541_1.fastq.gz | Fastqsanger.gz | |||
| SRR8580541_2.fastq.gz | Fastqsanger.gz | |||
| SRR8580542_1.fastq.gz | Fastqsanger.gz |
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Project description:In order to identify IFNα-induced host factor(s) that might inhibit replication of unadapted chimeric SIV/HIV-1 viruses (SHIVs), we measured IFNα-induced gene expression in immortalized pig-tailed macaque (Ptm) CD4+ lymphocytes. Triplicate cultures of Ptm lymphocytes were left untreated or treated with 1000 U/ml of IFNα. Twenty-four hours later, RNA was isolated, and RNA-seq libraries were prepared for sequencing. A total of 198 genes were found to be significantly differentially expressed (|logFC| ≥ 0.585 & FDR 5%) upon IFNα treatment. 147/198 genes were found to be significantly upregulated and 51/198 genes were found to be significantly downregulated regulated upon IFNα treatment.
2019-06-24 | GSE126594 | GEO
Project description:Macaque species share over 93% genome homology with humans and develop many disease phenotypes similar to those of humans, making them valuable animal models for the study of human diseases (e.g.,HIV and neurodegenerative diseases). However, the quality of genome assembly and annotation for several macaque species lags behind the human genome effort. To close this gap and enhance functional genomics approaches, we employed a combination of de novo linked-read assembly and scaffolding using proximity ligation assay (HiC) to assemble the pig-tailed macaque (Macaca nemestrina) genome. This combinatorial method yielded large scaffolds at chromosome-level with a scaffold N50 of 127.5 Mb; the 23 largest scaffolds covered 90% of the entire genome. This assembly revealed large-scale rearrangements between pig-tailed macaque chromosomes 7, 12, and 13 and human chromosomes 2, 14, and 15. We subsequently annotated the genome using transcriptome and proteomics data from personalized induced pluripotent stem cells (iPSCs) derived from the same animal. Reconstruction of the evolutionary tree using whole genome annotation and orthologous comparisons among three macaque species, human and mouse genomes revealed extensive homology between human and pig-tailed macaques with regards to both pluripotent stem cell genes and innate immune gene pathways. Our results confirm that rhesus and cynomolgus macaques exhibit a closer evolutionary distance to each other than either species exhibits to humans or pig-tailed macaques. These findings demonstrate that pig-tailed macaques can serve as an excellent animal model for the study of many human diseases particularly with regards to pluripotency and innate immune pathways.
2020-05-04 | PXD018943 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE17299: Direct effects of IFNα on human CD8 T cells_without any other concomitant signals GSE17301: The effect of IFNα on human CD8 T cells_with other concomitant signals Refer to individual Series
2010-07-23 | E-GEOD-17302 | biostudies-arrayexpress
Project description:Single-nucleus RNA sequencing (snRNA-seq) was used to profile the transcriptome of 7,631 nuclei in macaque adult testis. This dataset includes two samples from two different individuals. This dataset is part of a larger evolutionary study of adult testis at the single-nucleus level (97,521 single-nuclei in total) across mammals including 10 representatives of the three main mammalian lineages: human, chimpanzee, bonobo, gorilla, gibbon, rhesus macaque, marmoset, mouse (placental mammals); grey short-tailed opossum (marsupials); and platypus (egg-laying monotremes). Corresponding data were generated for a bird (red junglefowl, the progenitor of domestic chicken), to be used as an evolutionary outgroup.
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Project description:RNA expression in immortalized lymphocytes of schizophrenia and bipolar disorders patients were compared to that of their non-affected relatives to identify genes showing significant differences in expression. The study subjects were recruited in the Eastern Quebec kindred study.
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Project description:The primary goal of this study was to compare the performances of Rhesus Macaque Genome Array and Human Genome U133 Plus 2.0 Array with respect to the detection of differential expressions when rhesus macaque RNA extracts were labeled and hybridized. The secondary goal of this study was to investigate the effect of mismatch position on signal strength in Affymetrix GeneChips by examining naturally occurring mismatches between rhesus macaque transcripts and human probes from Human Genome U133 Plus 2.0 Array. The primary goal of this study was to compare the performances of Rhesus Macaque Genome Array and Human Genome U133 Plus 2.0 Array with respect to the detection of differential expressions when rhesus macaque RNA extracts were labeled and hybridized. The secondary goal of this study was to investigate the effect of mismatch position on signal strength in Affymetrix GeneChips by examining naturally occurring mismatches between rhesus macaque transcripts and human probes from Human Genome U133 Plus 2.0 Array. Keywords: cross hybridization Rhesus macaque RNA from five sources (immortalized fibroblasts, cerebral cortex, pancreas, testes and thymus) was divided into two sets of aliquots of equal amount. Samples from each of the five sources were labeled and hybridized with either Rhesus Macaque Genome Array or two Human Genome U133 Plus 2.0 Array. Rhesus macaque RNA from five sources (immortalized fibroblasts, cerebral cortex, pancreas, testes and thymus) was divided into two sets of aliquots of equal amount. Samples from each of the five sources were labeled and hybridized with either Rhesus Macaque Genome Array or two Human Genome U133 Plus 2.0 Array.
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Project description:The cause of systemic lupus erythematosus (SLE) is unknown. Interferonα (IFNα) has been suggested as a causative agent of SLE, however, it is not proven, and to what extent and how IFNα contributes to the disease is unknown. We here directly studied the contribution of IFNα to SLE by generating inducible IFNα transgenic mice which showed that conditional up-regulation of IFNα induced a typical manifestation of SLE including serum immune complex (IC), autoantibody against double stranded DNA (anti-dsDNA Ab) and the organ manifestations classical to SLE such as IC-deposited glomerulonephritis, classical splenic onion-skin lesion, and alopecia, epidermal liquefaction, positive lupus-band test of the skin. In the spleen of mice, activated effector CD4 T cells, interferonγ-producing CD8 T cells, B220+CD86+ cells and CD11c+CD86+ cells were increased, and the T cells produced increased amounts of IL-4, IL-6, IL-17 and IFNγ and decreased IL-2. In particular, activated CD3+CD4-CD8- double-negative T (DNT) cells positive for TCRαβ, B220, CD1d-teteramer, PD-1 and Helios, which produced increased amounts of IFNγ, IL-4, IL-17 and TNFα, were significantly expanded. They infiltrated into kidney and induced de novo glomerulonephritis and alopecia when transferred into naïve recipients. Thus, conditional up-regulation of IFNα is sufficient to induce SLE, and the DNT cells as expanded by IFNα are directly responsible for the organ manifestations such as lupus skin disease or nephritis.
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Project description:The RNA expression profile of retrovirally immortalized mature, murine T cells was compared to the expression profile of mature naive, murine T lymphocytes and/or murine thymocytes of healthy C57BL/6 mice. Retroviral insertional mutagenesis can contribute to immortalization of mature T lymphocytes, Newrzela et al. 2011 Mature T lymhpocytes were retrovirally immortalized. To compare the expression profile of immortalized T cells with non-manipulated wild type cells: RNA was isolated from fresh murine T lymphocytes, thymocytes and the immortalized T-cell population (each 1x10E7 cells). For naive T lymphocytes and thymocytes we used 8 weeks old C57BL/6 wild type (WT) donor animals. Study design: Prof. Dorothee von Laer. Study design and sample preparation: Dr.Sebastian Newrzela Gene expression profiling was performed as a commercial service by Miltenyi Biotec MACS molecular, Micorarray Service/ Cologne, Germany. Responsible scientist: Alena Fitz, Silvia Rüberg. Performed: March 2008
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Project description:Apolipoprotein A-I mimetic peptides are amphipathic alpha helix peptides that display similar functions to apolipoprotein A-I, and preclinical studies have evaluated . In this study, we evaluated the effect of the long-term expression of L37pA in the liver by an adeno-associated virus (AAV-L37pA) on the expression of an adeno-associated virus encoding interferon-alpha (AAV-IFNα). Long-term IFNα expression in the liver leads to lethal hematological toxicity one month after AAV administration. Concomitant administration of AAV-L37pA prevented the lethal toxicity since the IFNα expression was reduced one month after AAV administration by decreasing the expression of IFNα. To identify the mechanism of action of L37pA, a genomic and proteomic analysis was performed fifteen days after AAV administration when a similar level of IFNα and interferon-stimulated genes were observed in mice treated with AAV-IFNα alone and in mice treated with AAV-IFNα and AAV-L37pA. The coexpression of the apolipoprotein A-I mimetic peptide L37pA with IFNα modulated the gene expression program of IFNα, inducing a significant reduction in inflammatory pathways affecting pathogen-associated molecular patterns receptor, dendritic cells, NK cells and Th1 immune response. The proteomic analysis confirmed the impact of the L37pA activity on several inflammatory pathways and indicated an activation of LXR/RXR and PPPARα/γ nuclear receptors. Thus, long-term expression of L37pA induces an anti-inflammatory effect in the liver that allows silencing of IFNα expression mediated by an adeno-associated virus.
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