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Cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

ABSTRACT: Cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

PROVIDER: PRJNA642831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12108365.fastq.gz	Fastqsanger.gz
	SRR12108366.fastq.gz	Fastqsanger.gz
	SRR12108367.fastq.gz	Fastqsanger.gz
	SRR12108368.fastq.gz	Fastqsanger.gz
	SRR12108369.fastq.gz	Fastqsanger.gz

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Single cell profiling of cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

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Single cell profiling of cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

Project description:IL33 is a dual function cytokine which acts as a major orchestrator of the brain tumor microenvironment that contributes to tumorigenesis. We found that IL33 is expressed in a large subset of human glioma patient specimens and murine glioma models and that its expression is directly associated with the increased presence of tumor associated macrophages/monocytes/microglia. We analyzed the differences in the IL-33+ and IL-33- innate immune microenvironments at a single cell resolution and found substantial differences in the immune populations present and gene expression changes which may contribute to the increased tumoirgenicity of IL-33+ tumors.

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Cerebral immune cells in the Interleukin-33 (IL-33) driven tumor microenvironment

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Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

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A proteomic landscape of the spatiotemporal influence of Interleukin-33 (IL-33) in monocytes

Project description:Interleukin-33 (IL-33), a member of the IL-1 superfamily cytokines, is an endogenous danger signal and a nuclear-associated cytokine. It is one of the essential mediators of both innate and adaptive immune responses. Aberrant IL-33 signaling has been demonstrated to play a defensive role against various infectious and inflammatory diseases. Although the signaling responses mediated by IL-33 have been previously reported, the temporal signalingdynamicsare yet to be explored. Towards this end,we applied quantitative temporal phosphoproteomics analysis to elucidate pathways and proteins induced by IL-33 in THP1 monocytes. Employing TMT labeling-based quantitation and titanium dioxide (TiO2)-based phosphopeptide enrichment strategy followed by mass spectrometry analysis, we identified 14,515 phosphorylation sites mapping to 4,174 proteins across (0 min to 240 mins)time points.

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Dataset of spatiotemporal influences of interleukin IL-1 family cytokine: Interleukin-33 on cellular signal transduction pathways

Project description:Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that play a central role in the regulation of immune responses. IL-33 signaling, from the early signaling events triggered by the ligand-activated receptor to result in activation of early and late signaling events, such as proteome changes. In this study, THP1 (monocyte) cell line model was stimulated with IL-33 (50 ng/ml) for varying duration (5, 10, 15, 30, 40, 60, 120 and 240 mins). We carried out in-depth proteomic analysis using high-resolution LC-MS/MS. Our analysis resulted in the identification of 64,030 peptides corresponding to 7947 protein groups. Differentially regulated proteins identified in this study could be targeted for developing an inflammatory immune response.

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Project description:Tumor epithelial cells develop within a microenvironment consisting of extracellular matrix, growth factors, and cytokines produced by non-epithelial stromal cells. In response to paracrine signals from tumor epithelia, stromal cells modify the microenvironment to promote tumor growth and metastasis. Here, we identify interleukin (IL)-33 as an epithelial cell-derived regulator of stromal cell activation and mediator of intestinal polyposis. IL-33 expression was elevated in the tumors and serum of colorectal cancer patients and induced in the adenomatous polyps of ApcMin/+ mutant mice. Genetic and antibody suppression of IL-33 signaling in ApcMin/+ mice inhibited proliferation, induced apoptosis, and suppressed angiogenesis in polyps, which reduced both tumor number and size. In ApcMin/+ polyps, IL-33 expression localized to tumor epithelial cells and expression of the IL-33 receptor, IL1RL1, associated with two stromal cell types, namely subepithelial myofibroblasts (SEMFs) and mast cells, whose activation was previously associated with polyposis. In vitro IL-33 stimulation of human SEMFs induced the expression of extracellular matrix components and growth factors associated with intestinal tumor progression. IL-33 deficiency reduced mast cell accumulation in ApcMin/+ polyps and expression of mast cell-derived proteases and cytokines known to promote polyposis. Together, our results suggest that IL-33 is a tumor epithelial cell-derived paracrine signal that promotes polyposis through the coordinated activation of stromal cells and the formation of a reactive stroma microenvironment. Six T-75 flasks of CCD-18Co cells were grown to 80% confluency; three were treated with rhIL-33, three were given vehicle control; cells were trypsinized and split in two--half of each flask used for sequencing and half for qPCR validation post-sequencing

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Glioma-derived IL-33 orchestrates an inflammatory brain tumor microenvironment that accelerates glioma progression

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