While it is clear that T cell derived IFN has to act on tumor stroma cells for rejection of solid tumors, it is not clear which tumor stroma cells are targets. We studied how IFN affects gene expression in tumor blood vessels in vivo. To study the effect on endothelial cells, we either used a model of ectopic IFN (MCA313 tumors) or IFN-GFP fusion protein (J558L tumors) expression in tumors, or we used T cell derived IFN in large vascularized 16.113 tumours. Tumors were grown in mice that were expressing the IFN receptor ubiquitously (J558L tumors + IFN-GFP treatment and 16.113 tumors + T cell treatment) or in some experiments the IFN-receptor was expressed exclusively in endothelial cells (MCA313 tumor + IFN treatment).
Tumour ischaemia by interferon-γ resembles physiological blood vessel regression.
Sex, Specimen part, Time
View SamplesThis dataset is part of a study that investigated how the hematopoietic system coordinates the rapid and efficient regeneration of the megakaryocytic lineage during stress scenarios. We found that the phenotypic hematopoietic stem cell (HSC) compartment contains stem-like megakaryocyte-committed progenitors (SL-MkPs), a cell population that shares many features with multipotent HSCs and serves as a lineage-restricted emergency pool for inflammatory insults. This dataset contains single-cell RNA sequencing data of 30 hematopoietic stem and progenitor cells which, in the context of our study, confirmed that MK-specfic transcripts are of highly variable expression in HSCs. The dataset further showed that variations in MK transcript expression in HSCs is not correlated with global transcriptomic rearrangements. Overall design: Murine bone marrow cells were sorted by Lin-cKit+CD150+CD48- (referred to as cd150+ in the following) and Lin-cKit+CD150- (referred to as cd150- in the following). Transcriptomes of 11 cd150- and 9 cd150+ HSCs were determined using QUARTZ, a single-cell RNASeq protocol
Inflammation-Induced Emergency Megakaryopoiesis Driven by Hematopoietic Stem Cell-like Megakaryocyte Progenitors.
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View SamplesInduction of proximal components of the PI3-K/AKT pathway stimulates the expression of several genes, including several genes in the JAK/STAT pathway, documenting a crosstalk between these two important pathways.
STAT3 is a substrate of SYK tyrosine kinase in B-lineage leukemia/lymphoma cells exposed to oxidative stress.
Cell line, Treatment, Time
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