Following exposure to vaccines, antigen-specific CD8+ T-cell responses develop as long-term memory pools. Novel vaccine strategies based on adenoviral vectors, e.g. those developed for HCV, are able to induce and sustain substantial CD8+ T-cell populations. How such populations evolve following vaccination remains to be defined at a transcriptional level. We addressed the transcriptional regulation of divergent CD8+ T-cell memory pools induced by an adenoviral vector encoding a model antigen (beta-galactosidase). We observe transcriptional profiles that mimic those following infection with persistent pathogens, murine and human cytomegalovirus (CMV). Key transcriptional hallmarks include up-regulation of homing receptors, and anti-apoptotic pathways, driven by conserved networks of transcription factors, including T-bet (TBX21). In humans, a novel adenovirus vaccine induced similar CMV-like phenotypes and underlying transcription factor regulation. These data clarify the core features of CD8+ T-cell memory following vaccination with adenovirus vectors and indicate a conserved pathway for memory development shared with persistent herpesviruses.
Adenoviral Vector Vaccination Induces a Conserved Program of CD8(+) T Cell Memory Differentiation in Mouse and Man.
Specimen part
View SamplesTh17 cells were sorted ex vivo from PB of healthy donors as CD4+CD161+CCR6+CXCR3-. Following, cells were transduced with a lentiviral vector carrying the Eomes gene or with an empty vector. Infected cells were then enriched by MACS separation using the reporter gene NGFR as selection marker. Finally, cells were frozen for RNA analysis.
Eomes controls the development of Th17-derived (non-classic) Th1 cells during chronic inflammation.
Cell line
View SamplesInflammatory mediators play a role in the pathogenesis/progression of chronic heart failure (CHF). The aim of the present study was to identify diagnostic/prognostic markers and gene expression profiles of CHF vs control.
Gene expression profiles in peripheral blood mononuclear cells of chronic heart failure patients.
No sample metadata fields
View SamplesThe expression of a very large number of genes changes as male germ cells pass through differentiation into spermatids and then sperm. Much of this transcriptional programme requires the activity of the meiotic arrest genes.
The RNA export factor, Nxt1, is required for tissue specific transcriptional regulation.
Specimen part
View SamplesKeratinocytes isolated from one healthy donor were stimulated in triplicate for 24h with IL-36a, IL-36ß or IL-36? Overall design: Gene expression profile of IL-36 stimulated keratinocytes
An analysis of IL-36 signature genes and individuals with <i>IL1RL2</i> knockout mutations validates IL-36 as a psoriasis therapeutic target.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.
No sample metadata fields
View SamplesThe Cancer Cell Line Encyclopedia (CCLE) project is a collaboration between the Broad Institute, the Novartis Institutes for Biomedical Research and the Genomics Novartis Foundation to conduct a detailed genetic and pharmacologic characterization of a large panel of human cancer models
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Extrinsic Phagocyte-Dependent STING Signaling Dictates the Immunogenicity of Dying Cells.
Specimen part, Cell line
View SamplesThe ability of dying cells to activate antigen presenting cells (APCs) is carefully controlled to avoid unwarranted inflammatory responses. Here we show that engulfed cells only containing cytosolic dsDNA species (viral or synthetic) or cyclic di-nucleotides (CDNs) are able to stimulate APCs, via extrinsic STING-signaling.
Extrinsic Phagocyte-Dependent STING Signaling Dictates the Immunogenicity of Dying Cells.
Specimen part
View SamplesTransfected double strand DNA were required for the efficient activation of STING to activate innate immune cytokine.
Extrinsic Phagocyte-Dependent STING Signaling Dictates the Immunogenicity of Dying Cells.
Cell line
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