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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.
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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
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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.
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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.
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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
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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.
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these data demonstrate that GM-CSF levels during radiotherapy can be used as a prognostic biomarker for lung and esophageal cancer
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this study demonstrates that epithelial-derived GM-CSF is a critical early signal during allergic sensitization to cockroach allergen
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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.
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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
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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
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Results indicate GM-CSF as both a key contributor to the pathogenesis of MI and a potential therapeutic target.
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Obesity alters the lung neutrophil infiltration to enhance breast cancer metastasis through IL5 and GM-CSF.
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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.
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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.
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These findings describe a novel role for GM-CSF as an essential initiating cytokine in cardiac inflammation.
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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.
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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.
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IL-23-induced GM-CSF mediates the pathogenicity of CD4(+) T cells in experimental autoimmune myocarditis.
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GM-CSF accelerated the G1/S phase transition in EPCs by upregulating the expression of cyclins D1 and E.
