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anti-Human CSF2 Antikörper:
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Human Monoclonal CSF2 Primary Antibody für CyTOF, ELISA (Capture) - ABIN4899319
Hirst, Hallsworth, Peng, Lee et al.: Selective induction of eotaxin release by interleukin-13 or interleukin-4 in human airway smooth muscle cells is synergistic with interleukin-1beta and is mediated by the interleukin-4 receptor ... in American journal of respiratory and critical care medicine 2002
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Human Monoclonal CSF2 Primary Antibody für ELISA, WB - ABIN1724740
He, Shumansky, Connett, Anthonisen, Paré, Sandford: Association of genetic variations in the CSF2 and CSF3 genes with lung function in smoking-induced COPD. in The European respiratory journal 2008
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Human Monoclonal CSF2 Primary Antibody für FACS - ABIN4895921
Alisa, Boswell, Pathan, Ayaru, Williams, Behboudi: Human CD4(+) T cells recognize an epitope within alpha-fetoprotein sequence and develop into TGF-beta-producing CD4(+) T cells. in Journal of immunology (Baltimore, Md. : 1950) 2008
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Rat (Rattus) Monoclonal CSF2 Primary Antibody für CyTOF, FACS - ABIN4898951
Stojić-Vukanić, Nacka-Aleksić, Pilipović, Vujnović, Blagojević, Kosec, Dimitrijević, Leposavić: Aging diminishes the resistance of AO rats to EAE: putative role of enhanced generation of GM-CSF Expressing CD4+ T cells in aged rats. in Immunity & ageing : I & A 2015
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Mouse (Murine) Polyclonal CSF2 Primary Antibody für IHC (p), WB - ABIN3042527
Fang, Shi, Meng, Li, Peng: The Balance between Conventional DCs and Plasmacytoid DCs Is Pivotal for Immunological Tolerance during Pregnancy in the Mouse. in Scientific reports 2018
Human Polyclonal CSF2 Primary Antibody für FACS, IF - ABIN654647
Stone, Vanderman, Willey, Long, Register, Shively, Stehle, Loeser, Ferguson: Osteoarthritic changes in vervet monkey knees correlate with meniscus degradation and increased matrix metalloproteinase and cytokine secretion. in Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society 2015
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.
Data suggest that the methylotrophic yeast Pichia pastoris is an effective recombinant host for heterologous granulocyte-macrophage colony-stimulating factor (rhGM-CSF) production.
Letter: Knockdown of either filaggrin or loricrin increases the productions of interleukin (IL)-1alpha, IL-8, IL-18 and granulocyte macrophage colony-stimulating factor in stratified human keratinocytes.
Impaired RASGRF1/ERK-mediated GM-CSF response characterizes CARD9 deficiency in French-Canadians.
Honokiol could possess potential anti-inflammatory effects and inhibits TNF-alpha-induced IL-1beta, GM-CSF and IL-8 production in PBMCs from rheumatoid arthritis patients.
The canonical NFkappaB signaling in fibroblasts, but not in tumor cells, was shown to be responsible for the induced and constitutive CSF2 expression.
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.
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.
Evi1(+)DA-3 cells modified to express an intracellular form of GM-CSF, acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF levels.
IL-23-induced GM-CSF mediates the pathogenicity of CD4(+) T cells in experimental autoimmune myocarditis.
GM-CSF accelerated the G1/S phase transition in EPCs by upregulating the expression of cyclins D1 and E.
Proteomic Analysis Reveals Distinct Metabolic Differences Between Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) and Macrophage Colony Stimulating Factor (M-CSF) Grown Macrophages Derived from Murine Bone Marrow Cells
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