This SuperSeries is composed of the SubSeries listed below.
Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.
Sex, Age, Specimen part, Treatment
View SamplesHdac1 and 2 are important regulators of developmental processes. In this study we created microglia specific compound Hdac1 and Hdac2 knock out mice. Pre-natal ablation of both Hdac1 and 2 from microglia leads to reduced cell number and altered cell morphology. To investigate how Hdac1 and 2 knock out in microglia alters cellular gene expression profile we carried out RNA-seq analysis at different time points. Overall design: We used FACS sorted microglia cells from control and Hdac1/2fl/flCx3cr1Cre (constituitive knockout) or Hdac1/2fl/flCx3cr1CreERT2 (inducible) mice at different time points viz. Embryonic day 16 (E16 - inducible knockout only), Post natal day 0 (P0), 2 and 6 weeks after birth
Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.
Age, Treatment, Subject
View SamplesEpigenetic alterations has been implicated in the pathology of several neurodegenerative diseases. To investigate the role of microglial Hdac1 and 2 in the pathogenesis of Alzheimer's disease (AD), we created microglia specific compound Hdac1 and Hdac2 knock out mice in 5X FAD background. Genetic ablation of Hdac1 and 2 from microglia reduced amyloid plaque burden and improved spatial learning and memory function.
Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.
Sex, Specimen part
View SamplesAbstract: Immune subversion represents a hallmark of persistent infection, but microbial suppression of B cell responses remains mechanistically ill-defined. Adoptive transfer experiments in a chronic viral infection model evidenced the rapid and profound decimation of B cells that responded to virus or to concomitantly administered protein. Decimation affected naïve and memory B cells and resulted from biased differentiation into short-lived antibody-secreting cells. It was driven by type I interferon (IFN-I) signaling to several cell types including dendritic cells, T cells and myeloid cells. Durable B cell responses were restored upon IFN-I receptor blockade or, partially, when depleting myeloid cells or key IFN-I-induced cytokines. B cell decimation represents a molecular mechanism of humoral immune subversion and reflects an unsustainable “all-in” response of B cells in IFN-I-driven inflammation. Overall design: We adoptively transferred naïve KL25HL cells (LCMV-WE-GP-specific B cells) to aIFNAR- or isotype control-treated syngeneic recipient mice, followed by rLCMV-Cl13/WE-GP. On day 3 of infection, spleen were harvested and proliferated KL25HL B cell progeny (CD45.1+B220+CFSElo) were FACS-sorted and total RNA was processed for RNAseq. n=4
Interferon-driven deletion of antiviral B cells at the onset of chronic infection.
Age, Specimen part, Cell line, Subject
View SamplesPathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as damage-associated molecular patterns or alarmins, remains ill-defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8+ T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a MyD88-dependent, CTL-intrinsic fashion, determined polyfunctional effector cell differentiation and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses.
The alarmin interleukin-33 drives protective antiviral CD8⁺ T cell responses.
Specimen part
View SamplesPurpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goal of this study is to compare the transcriptome of OT-1 cells during priming (3 days after infection) and during effector phase ( 7 days after infection) in ODC-OVA mice after LCMV-OVA and Lm-OVA infection Overall design: OT-1 mRNA profiles of 7-weeks old ODC-OVA mice adoptively transfered with 10^5 OT-1 CD45.1 cells 3 and 7 days after i.v. infection with LCMV-OVA and Lm-OVA (deep sequencing, in triplicate, using Illumina).
Expression of the DNA-Binding Factor TOX Promotes the Encephalitogenic Potential of Microbe-Induced Autoreactive CD8<sup>+</sup> T Cells.
Cell line, Subject
View SamplesPurpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goal of this study is to compare the transcriptome of CNS-infiltrating OT-1 WT and Tox-deficient cells during effector phase (7 days after infection with LCMV-OVA) Overall design: OT-1 mRNA profiles of 7-weeks old ODC-OVA mice adoptively transfered with 10^5 OT-1 CD45.1 cells (WT and Tox-deficient) 7 days after i.v. infection with LCMV-OVA (deep sequencing, in triplicate, using Illumina).
Expression of the DNA-Binding Factor TOX Promotes the Encephalitogenic Potential of Microbe-Induced Autoreactive CD8<sup>+</sup> T Cells.
Cell line, Subject
View SamplesTo get more insight in cause and consequences of proteinuria, we studied glomerular gene expression patterns before and after the onset of increased urinary albumin excretion in a proteinuric rat strain.
Increased dynamin expression precedes proteinuria in glomerular disease.
No sample metadata fields
View SamplesProteome and transcriptome often show poor correlation, hindering the system-wide analysis of post-transcriptional regulation. Here, the authors study proteome and transcriptome dynamics during Drosophila embryogenesis and present basic mathematical models describing the temporal regulation of most protein-RNA pairs. Overall design: Whole embryos of Drosophila melanogaster measured at 14 time points during the first 20h of development (0h, 1h, 2h, 3h, 4h, 5h, 6h, 8h, 10h, 12h, 14h, 16h, 18h, 20h). Each sample was measured in biological quadruplicates. RNAseq samples correspond to proteome measurements deposited in ProteomeXchange as PXD005713.
Quantifying post-transcriptional regulation in the development of Drosophila melanogaster.
Specimen part, Cell line, Subject
View SamplesThe goal of the study is a high-throughput evaluation of the effect of TGFb treatment on gene expression.
Resolving the Combinatorial Complexity of Smad Protein Complex Formation and Its Link to Gene Expression.
Specimen part
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