IL 10 signalling and macrophage gene expression
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ABSTRACT:
PROVIDER: EGAS00001001283 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Study to stimulate WT and IL-10RB mutant macrophages with LPS in presence or absence of recombinant IL-10 and compare their gene expression profiles by RNASeq
These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ .
This dataset contains all the data available for this study on 2019-08-28.
| EGAD00001005300 | EGA
Project description:The experiments were done using an Orbitrap Fusion or an Orbitrap Fusion Lumos mass spectrometer. Multiplexing was achieved using either TMT10 or TMT11 reagents and the SPS-MS3 method. Basic pH reversed-phase chromatography (bRPLC) was used for off-line pre-fractionation; 12 fractions were analyzed for proteome mappings (PMID: 26700037) and 24 fractions plus a phosphotyrosine-enriched sample for phosphoproteome mappings (PMID: 31606085). Phosphoproteome mappings were done using both HCD fragmentation with Orbitrap fragment ion detection and CID fragmentation with ion trap fragment ion detection (PMID: 29487189, PMID: 31606085). If multiple TMT sets were required to analyze all samples from an experiment two bridge channels pooled from all samples was used to connect the data from the individual TMT sets (PMID: 28892078).
Five proteomics experiments are described in the paper:
(i) 1. Quantitative proteomics of fully polarized macrophages after 4 days of treatment with IL4 or IFNgamma/LPS to determine global proteome landscape of fully polarized THP-1-derived M1-type versus M2a-type macrophages:
Proteome mapping on Orbitrap Fusion (one TMT set)
RAW files: Marneros_4DayTreatment_proteome_fraction01 to ...fraction12
8 samples
Labeling: PMA.1 (126), PMA.2 (127n), IL4.1 (127c), IL4.2 (128n), ILJQ1.1 (128c), ILJQ1.2 (129n), IFNgamma.1 (129c), IFNgamma.2 (130n)
(ii) Time-course quantitative proteomics during the first 24 hours after induction of macrophage polarization in THP-1-derived macrophages to identify protein changes associated with M1-type (IFNgamma/LPS-induced) versus M2a-type (IL-4-induced) polarization:
Proteome mapping on Orbitrap Fusion (three TMT sets: set01, set02, set03)
RAW files:
Marneros_timecourse_proteome_TMTset01_fraction01 to ...fraction12
Marneros_timecourse_proteome_TMTset02_fraction01 to ...fraction12
Marneros_timecourse_proteome_TMTset03_fraction01 to ...fraction12
22 samples
Labeling:
set01; bridge 1 (126), PMA 0min (127n), PMA 10min (127c), PMA 30min (128n), PMA 1h (128c), PMA 2h (129n), PMA 4h (129c), PMA 8h (130n), PMA 24h (130c), bridge 2 (131n)
set02; bridge 1 (126), IL4 10min (127n), IL4 30min (127c), IL4 1h (128n), IL4 2h (128c), IL4 4h (129n), IL4 8h (129c), IL4 24h (130n), IFN 10min (130c), bridge 2 (131n)
set03; bridge 1 (126), IFN 30min (127n), IFN 1h (127c), IFN 2h (128n), IFN 4h (128c), IFN 8h (129n), IFN 24h (129c), bridge 2 (131n)
(iii) Time-course quantitative phosphoproteomics during the first 24 hours after induction of macrophage polarization in THP-1-derived macrophages to identify phosphorylation events associated with M1-type (IFNgamma/LPS-induced) versus M2a-type (IL-4-induced) polarization (same time points as in group 2):
Phosphoproteome mapping on Orbitrap Fusion (three TMT sets: set01, set02, set03)
RAW files:
Marneros_timecourse_phospho_TMTset01_fraction01 to ...fraction06, ...fraction08 to ...fraction24, ...pY
Marneros_timecourse_phospho_TMTset02_fraction01 to ...fraction12, ...fraction16 to ...fraction24, ...pY
Marneros_timecourse_phospho_TMTset03_fraction01 to ...fraction24, ...pY
The following RAW files gave no phosphopeptide quantifications (they are no included in the group of provided RAW files): set01_fraction07, set02_fraction13, set02_fraction14, set02_fraction15.
22 samples
Labeling: as in (ii)
(iv) Quantitative proteomics to assess the effects of the B-Raf inhibitor GDC-0879 or of the MEK inhibitor trametinib on IL-4-induced M2-type polarization and IFNgamma/LPS-induced M1-type polarization on THP-1-derived macrophages after 24 hours of treatment:
Proteome mapping on Orbitrap Fusion (one TMT set)
RAW files: Marneros_BRAF_inhibitor_proteine_fraction01 to ...fraction12
11 samples
Labeling: IL4 1 (131c), IL4 2 (127n), IL4+GDC 1 (131n), IL4+GDC 2 (128n), IL4+TRAM 1 (130c), IL4+TRAM 2 (129n), IFNgamma+LPS 1 (130n), IFNgamma+LPS 2 (127c), IFNgamma+LPS+TRAM 1 (126), IFNgamma+LPS+TRAM 2(129c), IFNgamma+LPS+GDC (128c)
(v) Quantitative phosphoproteomics to assess the effects of the B-Raf inhibitor GDC-0879 on IL-4-induced M2-type polarization and IFNgamma/LPS-induced M1-type polarization on THP-1-derived macrophages after 24 hours of treatment:
Phosphoproteome mapping on Orbitrap Fusion Lumos (one TMT set)
RAW files: Marneros_BRAF_inhibitor_phospho_fraction01 to ...fraction24, ...pY
7 samples
Labeling: IL4 1 (131c), IL4 2 (127n), IL4+GDC 1 (130n), IL4+GDC 2 (128n), IFNgamma+LPS 1 (128c), IFNgamma+LPS 2 (127c), IFNgamma+LPS+GDC (130c)
2019-12-10 | MSV000084672 | MassIVE
Project description:Study to investigate the transcriptional profile of suppressor CD4 T cells that express IL-10. IL-10-reporter mice were infected with mouse cytomegalovirus (MCMV) and activated IL-10+ and IL-10- cells were sorted from pooled salivary glands. RNA was extracted for RNA-seq analysis. These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2016-04-19 | E-ERAD-445 | biostudies-arrayexpress
Project description:Serine is a substrate for nucleotides, NADPH and glutathione (GSH) synthesis. Previous studies in cancer cells and lymphocytes have shown that serine-dependent one-carbon units are necessary for nucleotide production to support proliferation. Presently, it is unknown whether serine metabolism impacts the function of non-proliferative cells, such as inflammatory macrophages. We find that in macrophages, serine is required for optimal lipopolysaccharide (LPS) induction of IL-1β mRNA expression, but not inflammasome activation. The mechanism involves a requirement for glycine, which is made from serine, to support macrophage glutathione (GSH) synthesis. Cell-permeable GSH, but not the one-carbon donor formate, rescues IL-1β mRNA expression. Pharmacological inhibition of de novo serine synthesis in vivo decreased LPS induction of IL-1β levels and improved survival in an LPS-driven model of sepsis in mice. Our study reveals that serine metabolism is necessary for GSH synthesis to support IL-1β cytokine production.
2019-01-15 | GSE125036 | GEO
Project description:The objective was to determine the transcriptional effect of IL-17A on primary colonic epithelial cells in various differentiation states in vitro. The three states included 1) stem/progenitor cell spheroids grown in 50% L-WRN media as described in our previous publication (PMID: 24232249), 2) differentiating colonic epithelial spheroids (DM) placed in differentiation media without L-WRN for 24 hours, 3) terminally differentiated colonocyte spheroids placed in differentiation media without L-WRN for 48 hours as described in our previous publication (PMID: 27264604). Each condition was cultured with or without 20ng/ml recombinant mouse IL-17A for the final 24 hours.
2018-04-10 | E-MTAB-6365 | biostudies-arrayexpress
Project description:IL-10 or IL-6 stimulation of control 129xC57BL/6 murine bone marrow derived macrophages in the presence of LPS. We used microarrays to detail the global programme of gene expression changes in response to IL-6 or IL-10 stimulation in the presence of lipopolysaccharide. BMDMs were isolated from control, IL-6-/-, and IL-10-/- mice on a 129XBL/6 mixed background mice and differentiated in the presence of CSF-1 for 6-7 days. Cells were scraped and plated in 6 well plates at 2x10e6/well. Cells were washed with complete DMEM and rested for 1-2 hr before stimulation with combinations of IL-10 (10 ng/ml), IL-6 (2 ng/ml) or LPS (100 ng/ml) for 45 min or 180 mins. Complete biological replicates were performed. Experiment Overall Design: Data sets from wild-type, IL-10-/- and IL-6-/- BMDMs treated with IL-6 or IL-10 in the presence of LPS over time
2008-06-13 | E-GEOD-5589 | biostudies-arrayexpress
Project description:gene expression analysis through RNA sequencing of cultured bone marrow-derived WT, IRF5-/- or Csf2ra-/- eosinophils that were exposed or not to recombinant GM-CSF, IL-10 ot both overnight.
2021-06-17 | GSE145985 | GEO
Project description:It has been previously shown that airway exposure to Toll-like receptor ligands through lipopolysaccharide (LPS)-contaminated house dust or bacterial infections can exacerbate allergic inflammation; however, the underlying mechanism(s) controlling this response have not been fully elucidated. Here we report that basophils are the major source of Th2 cytokines that respond to TLR4 ligands, such as LPS and lipid A, in human PBMC and murine spleen cells. LPS activated human PBMCs to up-regulate mRNAs for not only pro-inflammatory cytokines such as IL-6 and chemokines such as CXCL8 (IL-8), CCL2 (MCP-1), but also Th2 cytokines such as IL-4 and IL13. Among PBMCs, we identified CD123+/BDCA4- basophils as the major source of IL-4 and IL-13 in response to LPS. Even in the absence of IgE, purified human basophils, as well as a basophilic cell line, were directly activated by LPS to produce IL-4 and IL-13. Moreover, LPS-stimulated IL-4 knockin mouse (4get mice) spleens identified the basophils as the major IL-4 producing cells in a TLR4-dependent manner. These results indicate that bacterial LPS may play a role in type-2 immunity through direct activation of basophils to produce IL-4 and IL-13. Keywords: Cell type comparison
2013-12-31 | GSE8589 | GEO
Project description:Effect of recombinant IL-33s, particularly IL-3395-270, IL-3399-270,IL-33109-270, and IL-33112-270 in HRMVECs
| PRJNA1029963 | ENA
Project description:IL-6 has been described to be a critical cytokine in mediating the febrile response because neither IL-6 knockout mice injected with peripheral lipopolysaccharide (LPS) or IL-1M-NM-2, nor animals treated with IL-6 antiserum develop fever. However, the fever response is developed in IL-6 KO mice following intracerebroventricular administration of Prostaglandin E2 which is the principal mediator of the febrile response. We performed a genome-wide microarray expression comparison between LPS-treated WT and IL-6 KO mice to evaluate if there were any differentially expressed genes in mice devoid of IL-6 that can explain the absence of fever response.
2012-10-29 | E-GEOD-34673 | biostudies-arrayexpress