Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteome of group 2 innate lymphoid cells (ILC2s) stimulated with IL33 and TL1A

ABSTRACT: We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.

INSTRUMENT(S): LTQ Orbitrap Velos, Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Primary Cell, Lung, Group 2 Innate Lymphoid Cell

SUBMITTER: Anne Gonzalez de Peredo

LAB HEAD: Anne Gonzalez de Peredo

PROVIDER: PXD041987 | Pride | 2024-03-05

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Experimental_design.txt	Txt
	OFMYC150416_02.raw	Raw
	OFMYC150416_04.raw	Raw
	OFMYC150416_06.raw	Raw
	OFMYC150416_13.raw	Raw

Items per page:

1 - 5 of 68

Similar Datasets

Mass spectrometry analysis of cleavage sites for different protease allergens in human IL-33

Project description:The cytokine interleukin-33 (IL-33) is an epithelial alarmin with critical roles in allergic inflammation and type 2 immunity. The project aims at the characterization of the direct cleavage of IL-33 by allergen proteases, resulting in its activation, and in the subsequent induction of type 2 cytokine production in group 2 innate lymphoid cells. The present dataset contains mass spectrometry analyses to map the cleavage sites for 9 distinct allergens proteases in the human IL-33 sequence.

2018-03-14 | PXD006081 | Pride

IL-33 induces a hypo-responsive human mast cell phenotype

Project description:Interleukin-33 (IL-33) is elevated in afflicted tissues of patients with mast cell-dependent chronic allergic diseases. Based on its acute effects on mouse mast cells (MCs), IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of chronic IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. We now find that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to antigen. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hypo-responsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation including antigen-mediated calcium mobilization and cytoskeletal reorganization; potentially as a consequence of down-regulation of the expression of PLCg1 and Hck. These findings suggest that IL-33 may play a protective, rather than a causative role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to down-regulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease. Mouse bone marrow-derived mast cells treated with IL3 or IL3+IL33. 6 replicates each.

2013-02-06 | E-GEOD-39382 | biostudies-arrayexpress

Single Cell based genomewide gene expression analysis of murine bone-marrow derived Very Small Embryonic-Like Stem Cells (VSELs)

Project description:Recently, we identified a population of Oct4+Sca-1+Lin-CD45- very small embryonic-like stem-cells (VSELs) in adult tissues. Open chromatin structure of pluripotency genes and genomic imprinting-related epigenetic mechanisms maintain pluripotency and quiescence of VSELs, respectively. However, global transcriptome signature of this rare stem-cell population remains elusive. Here, we demonstrate by genomewide gene-expression analysis with a small number of highly purified murine bone-marrow (BM)-derived VSELs, that Oct4+ VSELs i) express a similar, yet nonidentical, transcriptome as embryonic stem-cells (ESCs), ii) up-regulate cell-cycle checkpoint genes, iii) down-regulate genes involved in protein turnover and mitogenic pathways, and iv) highly express Ezh2, a polycomb group protein. Furthermore, as a result of Ezh2 overexpression, VSELs, like ESCs, exhibit bivalently modified nucleosomes (trimethylated H3K27 and H3K4) at promoters of important homeodomain-containing developmental transcription factors, thus preventing their premature transcription. Notably, spontaneous or RNA interference-enforced down-regulation of Ezh2 during VSEL differentiation removes the bivalent-domain (BD) structure, which leads to de-repression of several BD-regulated genes. Therefore, we suggest that VSELs, like other pluripotent stem-cells, maintain their pluripotent state through an Ezh2-dependent BD-mediated epigenetic mechanism. T7-primed cDNA libraries was synthesized using FACS sorted twenty cells. T7-primed libraries were biotin-labeled using the GeneChip 3’ in vitro transcription (IVT) kit (Affymetrix), starting from ‘‘In vitro Transcription to Synthesize Labeled aRNA. Nine Samples (3 VSELs, 3 HSC, and 3 ESC-D3) are analyzed using GeneChip 3’ Mouse Genome 430 2.0 array (Affymetrix), according to the manufacturer’s instructions.

2011-12-21 | E-GEOD-29281 | biostudies-arrayexpress

Quantitative phosphoproteomic analysis of IL-33 mediated signaling

Project description:Interleukin-33 (IL-33) is a novel member of the IL-1 family of cytokines that plays diverse roles in the regulation of immune responses. IL-33 exerts its effects by binding to a heterodimeric receptor complex consisting of interleukin-1 receptor like 1 (IL1RL1) and an accessory receptor protein IL-1RAcP resulting in the production and release of proinflammatory cytokines. A detailed understanding of the signaling pathways activated by IL-33 remains elusive. To elucidate IL-33 mediated signaling, we performed a global quantitative phosphoproteomic analysis using stable isotope labeling by amino acids in cell culture. Employing anti-phosphotyrosine antibodies and titanium dioxide-based enrichment strategies, we identified 6,207 phosphorylation sites mapping to 2,013 phosphoproteins of which more than 185 phosphosites are regulated by IL-33 stimulation. Our findings will greatly expand the understanding of IL-33 signaling and provide novel therapeutic targets for IL-33/IL-33R-associated diseases in humans.

2015-01-29 | PXD000984 | Pride

The transcription factor GATA3 is critical for the development of all IL-7Ra-expressing innate lymphoid cells (ILCs) and maintenance of type 2 ILCs

Project description:Innate lymphoid cells (ILCs) play critical roles during innate immune responses to pathogens and lymphoid organ development. IL-7Ra+ ILC subsets, similar to T helper (Th) cell subsets, produce distinctive effector cytokines. The molecular control of IL-7Ra+ ILC development and maintenance has yet to be dissected. Here we report that GATA3 is indispensable for the development of all IL-7Ra+ ILC subsets and T cells. Gata3 conditional deficient mice have no lymph nodes and are susceptible to Citrobactor rodentium infection. Genome-wide gene analyses indicate that GATA3 regulates similar set of cytokines and receptors in ILC2s and Th2 cells and is critical for the maintenance of ILC2s. Thus, GATA3 plays parallel roles in establishing and regulating both adaptive and innate lymphocytes. To identify GATA3 regulated genes in type 2 innate lymphoid cells by tamoxifen-mediated acute deletion of Gata3 gene.

2014-03-13 | E-GEOD-47851 | biostudies-arrayexpress

IL-2wt and IL-2nα differentially reshape the TME

Project description:Comparing two agonists of interleukin-2 (IL-2), IL-2wt and IL-2nα, differentially reshape the tumor microenvironment (TME). To more comprehensively explore the mechanisms by which the two different IL-2R agonists regulate the TME, we performed single-cell RNA sequencing (scRNA-seq) on immune cells isolated from tumors. We clustered the 18,455 tumor-infiltrating immune cells into 5 populations, and found marked expansion of T cell populations as well as contraction of mononuclear phagocyte populations in both IL-2wt and IL-2nα treated tumors compared with immunoglobulin G (IgG) controls.

2023-04-02 | E-MTAB-12373 | biostudies-arrayexpress

Top-down analysis of purified IL-38

Project description:Interleukin (IL)-1 family cytokines are essential for host defense at epithelial barriers. The IL-1 family member IL-33 was recently linked to stress granules (SGs). Formation of SGs and other biomolecular condensates is promoted by proteins containing low complexity regions (LCRs). Computational analysis predicted LCRs in six of the eleven IL-1 family members. Among these, IL-38 contained a long LCR including two amyloid cores. IL-38 localized to intracellular condensates in keratinocytes exposed to oxidative stress (OS) and formed OS-induced amyloid aggregates in cells and in vitro. Top-down proteomic analysis was performed on purified recombinant IL-38 protein to characterize the presence of possible disulfide bonds.

2024-11-03 | PXD052918 | Pride

IL-33 markedly induces murine eosinophil gene transcription via autocrine IL-4-dependent and -independent mechanisms

Project description:Eosinophils are major effector cells in type 2 inflammatory responses and become activated in response to IL-4 and IL-33, yet the molecular mechanism remains unclear. We examined the direct effect of these cytokines on eosinophils and demonstrated that murine eosinophils respond to IL-4 and IL-33 by phosphorylation of STAT-6 and NFkB, respectively. RNA sequencing analysis of murine eosinophils indicated that IL-33 regulates 519 genes, whereas IL-4 regulates only 28 genes, including 19 IL-33-regulated genes. Interestingly, IL-33 induced eosinophil activation via two distinct mechanisms, IL-4 independent and IL-4 secretion/auto-stimulation dependent. Anti-IL-4 or anti-IL-4Ra antibody-treated eosinophils, as well as Il4- or Stat6-deficient eosinophils, had attenuated protein secretion of a subset of IL-33-induced genes, including Retnla and Ccl17. However, the induction of most IL-33-regulated transcripts (e.g. Il6 and Il13) was IL-4 independent and blocked by NFkB inhibition. Indeed, IL-33 induced the rapid release of pre-formed IL-4 protein from eosinophils by an NFkB-dependent mechanism. Thus, we have identified a novel activation pathway in murine eosinophils that is induced by IL-33 and differentially dependent upon IL-4. These data suggest that IL-4 plays a critical role in auto-amplification of IL-33-induced eosinophil activation and could be a potential target for therapeutic approaches in IL-33-related eosinophil-associated diseases. Low density bone marrow derived murine eosinophils were generated in culture over the period of 14 days. Eosinophils were activated by either IL-33 or IL-4 at 10 ng/ml for 1hr and 4hr. RNA was collected and subjected to next generation sequencing.

2013-08-01 | E-GEOD-43660 | biostudies-arrayexpress

Peri-alloHCT IL-33 administration expands recipient T regulatory cells that protect mice against acute GvHD

Project description:Graft-versus-Host Disease (GvH) is the excessive inflammatory response by mature T cells contained in the graft during bone marrow transplantation. The allogeneic T cells recognize self-antigens as foreign and systemically attack multiple organs mostly with epithelial structures such as the skin, liver and gastrointestinal tract. We could show that IL-33 administration during allogeneic hematopoietic cell transplantation (alloHCT) increased regulatory T cell (Treg) numbers and ameliorated the outcome of GvHD. Furthermore, it is known that IL-33 also has an impact on myeloid cell compartments and we showed that IL-33 delivery together with a loss of FoxP3 positive Treg led to a massive expansion of myeloid cells. With the underlying experiment we wanted to further characterize the myeloid cells when Treg are lost, therefore mice were treated with IL-33 and one group had a loss in FoxP3 cells. CD11b+F4/80+Gr-1lo myeloid cells were sorted and analyzed in the microarray. The examined myeloid cell population shows strong activation of the IFNg transcriptome and are prone to M1 macrophage polarization. Therefore, Treg restrain myeloid cell expansion and polarization during IL-33 delivery.

2016-06-27 | E-MTAB-4677 | biostudies-arrayexpress

Expression data from mouse Nuocytes

Project description:Nuocytes are a recently described cell that responds to both IL-25 and IL-33 and produce high levels of IL-13 and IL-5 Mice were administered with 3 daily doses of IL-25 (400 ng/dose). Nuocytes were purified by flow cytometry. Spleen cells prepared from IL-25-treated mice were depleted of lineage+ cells before cell sorting by incubation with biotin-conjugated anti-CD3, anti-CD19, anti-CD11b and anti-FcεRI antibodies before removal of antibody-bound cells by magnetic separation using Dynabeads (Invitrogen). Lineage-depleted cells were stained with PE-conjugated antibodies against CD4, CD8, B220, TER-119 and CD11b, a FITC-conjugated antibody against CD45, and an APC-conjugated antibody against ICOS. PE−, FITC+, APC+ cells were collected using a Mo-flo cell sorter, and purity was checked by staining with lineage antibodies and antibodies against IL-17BR and T1/ST2. Following purification nuocytes were prepared directly for microarray gene expression analysis or cultured with IL-33 and IL-7 (both at 10 nanograms/ml) for 9 days before being prepared for microarray gene expression analysis.

2010-12-09 | E-GEOD-25890 | biostudies-arrayexpress

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