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Human CSF2 Protein expressed in Escherichia coli (E. coli) - ABIN2017902
Djalilian, Caicedo, Lessan, Grami, Le, Spellman, Pambuccian, Hall, Low, Ondrey: Efficacy of an osmotic pump delivered, GM-CSF-based tumor vaccine in the treatment of upper aerodigestive squamous cell carcinoma in rats. in Cancer immunology, immunotherapy : CII 2007
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Human CSF2 Protein expressed in Escherichia coli (E. coli) - ABIN803898
Carreño, Pacheco, Gutierrez, Jacobelli, Kalergis: Disease activity in systemic lupus erythematosus is associated with an altered expression of low-affinity Fc gamma receptors and costimulatory molecules on dendritic cells. in Immunology 2010
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Mouse (Murine) CSF2 Protein expressed in Escherichia coli (E. coli) - ABIN803901
Bråve, Ljungberg, Boberg, Rollman, Isaguliants, Lundgren, Blomberg, Hinkula, Wahren: Multigene/multisubtype HIV-1 vaccine induces potent cellular and humoral immune responses by needle-free intradermal delivery. in Molecular therapy : the journal of the American Society of Gene Therapy 2005
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Human CSF2 Protein expressed in Escherichia coli (E. coli) - ABIN934919
Spatz, Eibl, Hink, Wolf, Fischer, Mayr, Schernthaner, Eibl: Impaired primary immune response in type-1 diabetes. Functional impairment at the level of APCs and T-cells. in Cellular immunology 2003
It has been demonstrated that DLL1-dependent Notch signaling and GM-CSF cooperate to promote human dendritic cell differentiation.
Granulocyte-macrophage colony-stimulating factor inactivation in CAR T-cells prevents monocyte-dependent release of key cytokine release syndrome mediators.
GM-CSF and IL-2 provided the best yield to differentiate active TB from latent TB and from TB uninfected, respectively, however, neither was sensitive enough to be used as a stand-alone biomarker for active TB.
Study demonstrates that GM-CSF signaling is an important mechanism to tune macrophage inflammatory state and improve Mycobacterium tuberculosis (Mtb) control and that this pathway can be manipulated by pathogens to drive a more permissive bacterial state. Blocking GM-CSF makes macrophages more permissive of Mtb growth while addition of GM-CSF increases bacterial control.
characterizing GM-CSF and IL-3 as central mediators of innate immune activation is poised to open new therapeutic avenues for several immune-mediated disorders and define their potential in the context of immunotherapies.
GM-CSF could be induced by M. pneumoniae infection in vivo and vitro. Childen with high level GM-CSF had longer duration of fever. GM-CSF probably plays a vital role in neutrophil inflammation in M. pneumoniae infection.
Data show that CD4 T cells from synovial fluid are enriched for granulocyte-macrophage colony-stimulating factor (GM-CSF) production, suggests that the GM-CSF programme may be a primary pathogenic process.
GM-CSF bioavailability plays a critical role in maintaining intestinal homeostasis. Decreased bioavailability coupled with the genetic risk markers and/or smoking results in aggressive ileal Crohn's disease behavior.
Data show that GIF (ORF117 ) serves as a competitive decoy receptor by leveraging binding hotspots underlying the cognate receptor interactions of granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2).
As translated to human disease, these findings suggest vaccine-mediated expansion of GM-CSF-producing T cells could be an effective prophylactic or therapeutic TB strategy.
In a subset of patients who received GM-CSF, circulating myeloid-derived suppressor cells (MDSC), and anti-GM-CSF-neutralizing antibodies (Nabs) were also modulated. The majority of patients developed anti-GM-CSF Nabs, which correlated with improved RFS and OS
this study shows that cortisol inhibits CSF2 via DNA methylation and inhibits invasion in first-trimester trophoblast cells
Upregulation of GM-CSF and M-CSF production by endothelial cells, an effect that appears to be mediated by NF-kappaB and to be independent of IL-1, may be an additional mechanism through which IL-33 contributes to inflammatory activation of the vessel wall.
Oral and periodontal innate immunity is affected by HIV viremia and ART. GCF IL-8, G-CSF, as well as serum IL-8, MCP-1 and GM-CSF may be useful biomarkers for the detection of disease presence and/or its severity due to HIV infection and ART use.
This review summarizes a number of findings to provide the currently available information regarding the anticancer immune response of GM-CSG. [review]
Data suggest that the intratumoral GM-CSF expression, as a potentially independent prognostic biomarker for recurrence, might improve conventional clinical and pathologic analysis to refine outcome prediction for clinically localized clear-cell renal cell carcinoma (ccRCC) patients after surgery.
High GM-CSF expression is associated with breast Cancer.
In gastric cancer (GC), tumour-derived GM-CSF activated neutrophils and induced neutrophil PD-L1 expression via Janus kinase (JAK)-signal transducer and activator of transcription 3 (STAT3) signalling pathway. The activated PD-L1(+) neutrophils effectively suppressed normal T-cell immunity in vitro and contributed to the growth and progression of human GC in vivo.
The IL-3/ GM-CSF effected on the myofibroblastic differentiation of human adipose derive stromal cells (hASCs) as well as it did on human dermal fibroblasts (HDFs).
Obesity alters the lung neutrophil infiltration to enhance breast cancer metastasis through IL5 and GM-CSF.
TRAF6 is also required for GM-CSF-induced ubiquitination and activation of Akt.
CSF2 stimulates proliferation of trophectoderm cells by activation of the PI3K-and ERK1/2 MAPK-dependent MTOR signal transduction cascades.
The data solidify GM-CSF as a fundamental pathogenic driver of tissue inflammation, in particular, GM-CSF expression is a signature cytokine of a distinct pathogenic T Helper subset in neuroinflammation.
interaction of HuR and miR-466i orchestrates GM-CSF expression in Th17 cells
Endoplasmic reticulum stress in Perivascular adipose tissue destabilizes atherosclerotic plaque, in part through increasing GM-CSF paracrine via transcription factor NF-kappaB.
The data of this study indicated that GM-CSF is a proinflammatory cytokine that contributes to nociceptive signalling through driving spinal glial cell secretion of proinflammatory mediators.
Data show that the microbiota enhances respiratory defenses via granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling, which stimulates pathogen killing and clearance by alveolar macrophages
The data indicate that GM-CSF drives chronic tissue damage and disability in experimental autoimmune encephalomyelitis via pleiotropic pathways, but it is dispensable during early lesion formation and the onset of neurologic deficits.
the release of IL-33 and GM-CSF from epithelial cells induces the activation of p65 and the p38-MK2/3 signaling module in Dendritic Cells, resulting in Th2 polarization and, finally, allergic inflammation.
results show T cell production of GM-CSF contributes to control of M. tuberculosis infection in the absence of other sources of GM-CSF, that multiple T cell subsets make GM-CSF in the lung over the course of infection and that GM-CSF can act directly on infected macrophages through a pathway requiring PPARgamma to limit bacterial growth
In conclusion, our study confirms the pathogenic role of GM-CSF in colitis-associated colorectal cancer development. GM-CSF favors tumor-permissive microenvironment by inducing MDSC generation and recruiting them into colonic tissues.
these data demonstrate that GM-CSF levels during radiotherapy can be used as a prognostic biomarker for lung and esophageal cancer
this study demonstrates that epithelial-derived GM-CSF is a critical early signal during allergic sensitization to cockroach allergen
These impaired macrophage functions in leukemic mice were significantly corrected by IL-3 and GM-CSF treatment indicating the therapeutic benefit of these two cytokines in leukemia.
Both IL-6 protein production and transcript levels were downregulated by RA in respiratory tract epithelial cells (LETs) , but upregulated in macrophages (MACs). RA also increased transcript levels of MCP-1, GMCSF, and IL-10 in MACs, but not in LETs. Conversely, when LETs, but not MACs, were exposed to RA
T-GM-CSF and -IL-3 significantly, and reciprocally, blunted receptor binding and myeloid progenitor cell proliferation activity of both FL-GM-CSF and -IL-3 in vitro and in vivo
Results indicate GM-CSF as both a key contributor to the pathogenesis of MI and a potential therapeutic target.
GM-CSF is required for the normal balance of leukocyte subsets, including granulocytes, B cells, and naive vs. effector T cells. There was an approximately 3-fold increase in the percentages of granulocytes in Csf2-/- PBMCs. The presence of maximal experimental autoimmune encephalomyelitis in the complete absence of GM-CSF revealed that GM-CSF is not an obligate effector molecule in all forms of EAE.
chemerin inhibited nuclear factor-kappaB activation and the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-6) by tumor cells and tumor-associated endothelial cell, respectively, via its receptors, and consequently, MDSC induction was impaired, leading to restoration of antitumor T-cell response and decreased tumor angiogenesis.
These findings describe a novel role for GM-CSF as an essential initiating cytokine in cardiac inflammation.
Data reviewed establish that any damage to brain tissue tends to cause an increase in G-CSF and/or GM-CSF (G(M)-CSF) synthesized by the brain. Glioblastoma cells themselves also synthesize G(M)-CSF. G(M)-CSF synthesized by brain due to damage by a growing tumor and by the tumor itself stimulates bone marrow to shift hematopoiesis toward granulocytic lineages away from lymphocytic lineages.
It was concluded that CSF2 can act as a developmental programming agent but alone is not able to abolish the adverse effects of in vitro production on fetal characteristics.
These results demonstrated that bovine colonic cells seem capable to respond to E. bovis merozoite I infection by the upregulation of CXCL10 and GM-CSF gene transcription.
Data suggest exposure to maternal CSF2 from D5-D7 of development is fundamentally different for female/male blastocysts with respect to embryo elongation, characteristics of transcriptome/methylome, and endometrial interferon tau secretion at D15.
inhibits induction of apoptosis in the bovine preimplantation embryo
The increase in calving rate caused by CSF2 treatment involves, in part, more extensive development of extraembryonic membranes and capacity of the conceptus to secrete IFNT2 at day 15 of pregnancy.
immunolocalization studies confirmed the presence of granulocyte-macrophage colony stimulating factor(GM-CSF) in the germ cell line in bovine and human testes and addition of GM-CSF enhances several parameters of sperm motility
the conceptus, through its secretion of IFN-tau, stimulates maternal epithelial expression of COX-2 and GM-CSF during the peri-attachment period in the cow.
CSF2 affect embryonic development and enhance embryo competence for posttransfer survival.
Data indicate that differentially expressed IL-17, IL-22, and IL-23 levels are associated with K-ras in a stage-specific fashion along colorectal cancer progression and an association was established between mutant K-ras and GM-CSF and IFN-gamma.
The protein encoded by this gene is a cytokine that controls the production, differentiation, and function of granulocytes and macrophages. The active form of the protein is found extracellularly as a homodimer. This gene has been localized to a cluster of related genes at chromosome region 5q31, which is known to be associated with interstitial deletions in the 5q- syndrome and acute myelogenous leukemia. Other genes in the cluster include those encoding interleukins 4, 5, and 13.
, granulocyte-macrophage colony-stimulating factor
, colony stimulating factor 2 (granulocyte-macrophage)
, colony-stimulating factor
, granulocyte-macrophage colony stimulating factor 2
, put. GM-CSF
, granulate-macrophage stimulating factor
, granulocyte-macrophage stimulation factor