Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112369 | ENA |
REPOSITORIES: ENA
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Project description:GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B. To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells. Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. CMPs were isolated and cultured with GM-CSF.
2010-02-02 | GSE14698 | GEO
Project description:GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B. To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells. Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. CMPs were isolated and cultured with GM-CSF. Experiment Overall Design: Microarray Experiments for mice lacking or with the Stat5a and 5b genes in blood cells that were treated w/o CMP
2010-02-21 | E-GEOD-14698 | biostudies-arrayexpress
Project description:GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B. To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells. Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. GMPs were isolated and cultured with GM-CSF. Both the number and size of STAT5A/B-null colonies were reduced and GM-CSF-induced survival of mature STAT5A/B-null neutrophils was impaired. Time-lapse cinematography and single cell tracking of GMPs revealed that STAT5A/B-null cells were characterized by a longer generation time and an increased cell death. Gene expression profiling experiments suggested that STAT5A/B directs GM-CSF signaling through the regulation of cell survival genes.
2009-09-30 | GSE14672 | GEO
Project description:GM-CSF controls the development of granulocytes but little is known about the contribution of the downstream mediating transcription factor STAT5A/B. To elucidate this pathway, we generated mice lacking the Stat5a and 5b genes in blood cells. Peripheral neutrophils were decreased and administration of 5-FU and GM-CSF failed to induce granulopoiesis in Stat5a/b-mutant mice. GMPs were isolated and cultured with GM-CSF. Both the number and size of STAT5A/B-null colonies were reduced and GM-CSF-induced survival of mature STAT5A/B-null neutrophils was impaired. Time-lapse cinematography and single cell tracking of GMPs revealed that STAT5A/B-null cells were characterized by a longer generation time and an increased cell death. Gene expression profiling experiments suggested that STAT5A/B directs GM-CSF signaling through the regulation of cell survival genes. Experiment Overall Design: Mice lacking or with the Stat5a and 5b genes in blood cells, which were treated w/o GMP
2009-10-10 | E-GEOD-14672 | biostudies-arrayexpress
Project description:Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. Multiple factors including cytokines, transcription factors and multiple signaling pathways are involved in MDSC differentiation. Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin(IL-6) etc could in vitro mediate development of MDSCs.IL-6 with GM-CSF mediated MDSC not only had stronger suppressive function but also the dynamics of their suppressive function was different from GM-CSF alone mediated MDSCs.To found a new regulatory factor (s) in tumor and inflammatory environments, we compared GM-CSF and IL-6 mediated MDSCs with GM-CSF alone mediated MDSCs using lncRNA microarray and protein-coding mRNA microarrays.
2017-10-09 | GSE104718 | GEO
Project description:Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. Multiple factors including cytokines, transcription factors and multiple signaling pathways are involved in MDSC differentiation. Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin(IL-6) etc could in vitro mediate development of MDSCs.IL-6 with GM-CSF mediated MDSC not only had stronger suppressive function but also the dynamics of their suppressive function was different from GM-CSF alone mediated MDSCs.To found a new regulatory factor (s) in tumor and inflammatory environments, we compared GM-CSF and IL-6 mediated MDSCs with GM-CSF alone mediated MDSCs using lncRNA microarray, miRNA microarrays and protein-coding mRNA microarrays.
2017-10-09 | GSE104719 | GEO
Project description:GM-CSF is involved in immune complex (IC)-mediated arthritis. However, little is known about what is the cellular source of GM-CSF and how it is regulated during IC-mediated inflammation. Using novel GM-CSF reporter mice, we show that NK cells produce GM-CSF during an IC-mediated model of inflammatory arthritis. NK cells promoted STIA in a GM-CSF-dependent manner, as deletion of NK cells and selective removal of GM-CSF production by NK cells abrogated disease. Furthermore, we show that myeloid cell activation by GM-CSF is restrained by induction of JAK/STAT checkpoint inhibitor cytokine-inducible SH2-containing protein, CIS. Myeloid cells from CIS-deficient mice had exaggerated responses to GM-CSF, and these mice develop exacerbated STIA. Our data suggest that tissue NK cells may amplify joint inflammation in arthritis via GM-CSF production and thus represent a novel target in IC-mediated pathology. Endogenous CIS provides a key brake on signaling through the GM-CSF receptor and strategies that boost its function may provide an alternative anti-inflammatory approach.
2020-02-19 | PXD012794 | Pride
Project description:Pseudomonas aeruginosa PAO1 persister and normal cells were treated with and without Granulocyte Macrophage Colony-Stimulating Factor (GM-CSF) to understand the effect of GM-CSF on gene expression of PAO1. We used DNA microarrays to identify the down-regulated and up-regulated genes after GM-CSF treatment.
2014-11-25 | GSE63588 | GEO
Project description:Inhibition of STAT5 was recently reported to reduce mouse atherosclerosis. However, the regulatory role of STAT5 isoforms STAT5A and STAT5B in human disease and more specifically in macrophages remains unknown. Here, we demonstrate reciprocal expression regulation of STAT5A and B in human atherosclerotic lesions. The former was highly upregulated in ruptured over stable plaque and correlated with macrophage presence, a finding that was corroborated by the high chromosomal accessibility of STAT5A but not B gene in plaque macrophages. Phosphorylated STAT5 correlated with macrophages confirming its activation status. As macrophage STAT5 is activated by GM-CSF, we studied the effects of its silencing in GM-CSF differentiated human macrophages. STAT5A knockdown blunted NF-kB pathway, phagocytosis, cholesterol metabolism, and apoptosis terms. These changes at transcriptional level could be confirmed at functional level, with significant increases in apoptosis and phagocytosis and decreases in lipid uptake and IL-6, IL8, and TNFa cytokine secretion after STAT5A knockdown. Finally, inhibition of general and isoform A specific STAT5 inhibitor significantly reduced the secretion of TNFa, IL-8 and IL-10 in ex vivo tissue slices of advanced human atherosclerotic plaques. In summary, we identify STAT5A as important determinant of macrophage functions and inflammation in the context of atherosclerosis and show its promise as therapeutic target for human atherosclerotic plaque inflammation.
2023-10-02 | GSE217893 | GEO
Project description:Modelling combined virotherapy and immunotherapy:strengthening the antitumour immune response mediated byIL-12 and GM-CSF expression
Adrianne L. Jennera, Chae-Ok Yunb, Arum Yoonb, Adelle C. F. Costercand Peter S. Kimaa
School of Mathematics and Statistics, University of Sydney, Sydney, Australia;bDepartment ofBioengineering, Hanyang University, Seoul, Korea;cSchool of Mathematics and Statistics, University of NewSouth Wales, Sydney, Australia
ABSTRACT
Combined virotherapy and immunotherapy has been emergingas a promising and effective cancer treatment for some time.Intratumoural injections of an oncolytic virus instigate an immunereaction in the host, resulting in an influx of immune cells tothe tumour site. Through combining an oncolytic viral vector withimmunostimulatory cytokines an additional antitumour immuneresponse can be initiated, whereby immune cells induce apoptosisin both uninfected and virus infected tumour cells. We developa mathematical model to reproduce the experimental results fortumour growth under treatment with an oncolytic adenovirus co-expressing the immunostimulatory cytokines interleukin 12 (IL-12)and granulocyte-monocyte colony stimulating factor (GM-CSF). Byexploring heterogeneity in the immune cell stimulation by thetreatment, we find a subset of the parameter space for the immunecell induced apoptosis rate, in which the treatment will be lesseffective in a short time period. Therefore, we believe the bivariatenature of treatment outcome, whereby tumours are either completelyeradicated or grow unbounded, can be explained by heterogeneity inthis immune characteristic. Furthermore, the model highlights theapparent presence of negative feedback in the helper T cell and APCstimulation dynamics, when IL-12 and GM-CSF are co-expressed asopposed to individually expressed by the viral vector.
2020-01-09 | MODEL1912120003 | BioModels