Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE153489 | GEO | 2020/08/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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.

2020-08-21 | GSE153487 | GEO

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

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

| PRJNA642831 | ENA

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

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

| PRJNA642837 | ENA

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

Project description:To validate the modulation of inflammatory genes by ectopic IL-33, we performed Gene expression analysis using the nCounter Mouse v2 Inflammation Panel. This result validated a significant increase in a number of anti-inflammatory cytokines in the IL-33+ xenografts that were absent in the DNLS xenografts

2020-08-21 | GSE153488 | GEO

Interleukin-33 in experimental kidney fibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-05-06 | GSE149918 | GEO

Identification of constitutively active interleukin 33 (IL-33) splice variant.

Project description:IL-33/IL-1F11 is a new member of the IL-1 family ligand and provokes T helper-type immune responses. IL-33 is the ligand of ST2 and IL-1 receptor accessory protein (IL-1RAcP) that triggers nuclear factor-κ light chain enhancer of activated B cells (NF-κB) and MAPK signaling. We discovered a novel short splice variant of IL-33 that was termed spIL-33. The new spIL-33 lacks exon 3 containing a proposed caspase-1 cleavage site. We isolated spIL-33 cDNA from the Huh7 human hepatocarcinoma cell line and expressed the recombinant spIL-33 protein in Escherichia coli. The recombinant spIL-33 and pro-IL-33 were not cleaved by caspase-1, unlike IL-18 (IL-1F4). The recombinant spIL-33 was constitutively active, and spIL-33-induced inflammatory cytokine production was caspase-1-independent in HMC-1 and Raw 264.7 cells. The recombinant spIL-33 induced the phosphorylation of IL-1 receptor-associated kinase (IRAK1), NF-κB, p38 MAPK, p44/42 MAPK, and JNK in a time- and dose-dependent manner. Anti-ST2 monoclonal antibody specifically blocked the spIL-33-induced cytokine production. In this study, we identified and characterized a new IL-33 splice variant, which was a constitutively active IL-33 isoform. The existence of constitutively active spIL-33 suggests that the biological activity of IL-33 could be triggered by diverse stimulations during immune responses. Further investigation of the spIL-33 expression pattern may contribute to understanding the involvement of IL-33 in inflammatory disorders.

| S-EPMC3103380 | biostudies-literature

Collagen-anchored interleukin-2 and interleukin-12 safely reprogram the tumor microenvironment in soft tissue sarcomas

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-01 | GSE218914 | GEO

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

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

| PRJNA642836 | ENA

The Contradictory Role of Interleukin-33 in Immune Cells and Tumor Immunity.

Project description:Interleukin (IL)-33 is a member of the IL-1 superfamily and is a crucial cytokine playing the role of a dual-function molecule. IL-33 mediates its function by interacting with its receptor suppression of tumorigenicity 2 (ST2), which is constitutively expressed on T helper (Th)1 cells, Th2 cells, and other immune cells. Previously, we summarized ?ndings on IL-33 and performed an intensive study of the correlation between IL-33 and tumor. IL-33 enables anti-tumor immune responses through Th1 cells and natural killer (NK) cells and plays a role in tumor immune escape in cancers via Th2 cells and regulatory T cells. Herein, we discuss the contradictory role of IL-33 in immune cells in different cancer, and our summaries may be helpful for better understanding of the development of research on IL-33 and tumor immunity.

| S-EPMC7457384 | biostudies-literature

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

Project description:Despite a deeper molecular understanding, human glioblastoma remains one of the most treatment refractory and fatal cancers. It is known that the presence of macrophages and microglia impact glioblastoma tumorigenesis and prevent durable response. Herein we identify the dual function cytokine IL-33 as an orchestrator of the glioblastoma microenvironment that contributes to tumorigenesis. We find that IL-33 expression in a large subset of human glioma specimens and murine models correlates with increased tumor-associated macrophages/monocytes/microglia. In addition, nuclear and secreted functions of IL-33 regulate chemokines that collectively recruit and activate circulating and resident innate immune cells creating a pro-tumorigenic environment. Conversely, loss of nuclear IL-33 cripples recruitment, dramatically suppresses glioma growth, and increases survival. Our data supports the paradigm that recruitment and activation of immune cells, when instructed appropriately, offer a therapeutic strategy that switches the focus from the cancer cell alone to one that includes the normal host environment.

| S-EPMC7536425 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data