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Journal articles on the topic 'GM-CSF'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Sands, Bruce E. "GM-CSF." Inflammatory Bowel Diseases 12 (April 2006): S12. http://dx.doi.org/10.1097/00054725-200604002-00024.

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Ratto, Alessandra, Claudio Petterino, Tullio Florio, and Federica Barbieri. "Goat anti-human GM-CSF recognizes canine GM-CSF." Veterinary Clinical Pathology 41, no. 1 (2012): 3–4. http://dx.doi.org/10.1111/j.1939-165x.2012.00407.x.

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3

&NA;. "DT388-GM-CSF." Inpharma Weekly &NA;, no. 1152 (1998): 7. http://dx.doi.org/10.2165/00128413-199811520-00012.

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4

Senzer, N., C. Bedell, and J. Nemunaitis. "OncoVEX(GM-CSF)." Drugs of the Future 35, no. 6 (2010): 449. http://dx.doi.org/10.1358/dof.2010.035.06.1500437.

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Senzer, N., C. Bedell, and J. Nemunaitis. "OncoVEX(GM-CSF)." Drugs of the Future 35, no. 6 (2010): 449. http://dx.doi.org/10.1358/dof.2010.35.6.1500437.

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6

McNiece, I., R. Andrews, M. Stewart, S. Clark, T. Boone, and P. Quesenberry. "Action of interleukin-3, G-CSF, and GM-CSF on highly enriched human hematopoietic progenitor cells: synergistic interaction of GM-CSF plus G-CSF." Blood 74, no. 1 (1989): 110–14. http://dx.doi.org/10.1182/blood.v74.1.110.110.

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Abstract Purified preparations of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and interleukin 3 (IL-3 or multi-CSF) alone and in combination, have been compared for their stimulatory effects on human granulocyte-macrophage colony forming cells (GM-CFC). In cultures of unseparated normal human bone marrow, the combinations of G-CSF plus IL-3 and GM-CSF plus IL-3 stimulated additive numbers of GM colonies, while GM-CSF plus G-CSF stimulated greater than additive numbers of GM colonies, compared with the sum of the colony formation obtaine

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McNiece, I., R. Andrews, M. Stewart, S. Clark, T. Boone, and P. Quesenberry. "Action of interleukin-3, G-CSF, and GM-CSF on highly enriched human hematopoietic progenitor cells: synergistic interaction of GM-CSF plus G-CSF." Blood 74, no. 1 (1989): 110–14. http://dx.doi.org/10.1182/blood.v74.1.110.bloodjournal741110.

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Purified preparations of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and interleukin 3 (IL-3 or multi-CSF) alone and in combination, have been compared for their stimulatory effects on human granulocyte-macrophage colony forming cells (GM-CFC). In cultures of unseparated normal human bone marrow, the combinations of G-CSF plus IL-3 and GM-CSF plus IL-3 stimulated additive numbers of GM colonies, while GM-CSF plus G-CSF stimulated greater than additive numbers of GM colonies, compared with the sum of the colony formation obtained with ea

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8

Reed, Jacquelyn A., Machiko Ikegami, Eli R. Cianciolo, et al. "Aerosolized GM-CSF ameliorates pulmonary alveolar proteinosis in GM-CSF-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 4 (1999): L556—L563. http://dx.doi.org/10.1152/ajplung.1999.276.4.l556.

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Surfactant proteins and phospholipids accumulate in the alveolar spaces and lung tissues of mice deficient in granulocyte-macrophage colony-stimulating factor (GM-CSF), with pathological findings resembling the histology seen in the human disease pulmonary alveolar proteinosis (PAP). Previous metabolic studies in GM-CSF-deficient [GM(−/−)] mice indicated that defects in surfactant clearance cause the surfactant accumulation in PAP. In the present study, GM(−/−) mice were treated daily or weekly with recombinant mouse GM-CSF by aerosol inhalation or intraperitoneal injection for 4–5 wk. Lung hi

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9

Tazawa, Ryushi, and Koh Nakata. "GM-CSF Therapy for Pulmonary Alveolar Proteinosis." Nihon Naika Gakkai Zasshi 99, no. 7 (2010): 1623–27. http://dx.doi.org/10.2169/naika.99.1623.

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10

Frossard, Jean Louis, Ashok K. Saluja, Nicolas Mach, et al. "In vivo evidence for the role of GM-CSF as a mediator in acute pancreatitis-associated lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 3 (2002): L541—L548. http://dx.doi.org/10.1152/ajplung.00413.2001.

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Severe pancreatitis is frequently associated with acute lung injury (ALI) and the respiratory distress syndrome. The role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in mediating the ALI associated with secretagogue-induced experimental pancreatitis was evaluated with GM-CSF knockout mice (GM-CSF −/−). Pancreatitis was induced by hourly (12×) intraperitoneal injection of a supramaximally stimulating dose of the cholecystokinin analog caerulein. The resulting pancreatitis was similar in GM-CSF-sufficient (GM-CSF +/+) control animals and GM-CSF −/− mice. Lung injury, quantitated

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11

Campbell, Ian K., Melissa J. Rich, Robert J. Bischof, Ashley R. Dunn, Dianne Grail, and John A. Hamilton. "Protection from Collagen-Induced Arthritis in Granulocyte-Macrophage Colony-Stimulating Factor-Deficient Mice." Journal of Immunology 161, no. 7 (1998): 3639–44. http://dx.doi.org/10.4049/jimmunol.161.7.3639.

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Abstract The involvement of granulocyte-macrophage CSF (GM-CSF) in collagen-induced arthritis (CIA) was examined using GM-CSF-deficient mice. Although CIA is generally considered to be restricted to mice of the H-2q or H-2r haplotypes, we examined the role of GM-CSF in the CIA model using GM-CSF-deficient (−/−) and wild-type (+/+) mice on a C57BL/6 (H-2b) background. Mice were immunized by intradermal injection at the base of the tail with chick type II collagen followed by a repeat injection 21 days later. We found, based on both clinical and histologic assessments, that wild-type mice on thi

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12

Ballinger, Megan N., Leah L. N. Hubbard, Tracy R. McMillan, et al. "Paradoxical role of alveolar macrophage-derived granulocyte-macrophage colony-stimulating factor in pulmonary host defense post-bone marrow transplantation." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 1 (2008): L114—L122. http://dx.doi.org/10.1152/ajplung.00309.2007.

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Impaired host defense post-bone marrow transplant (BMT) is related to overproduction of prostaglandin E2(PGE2) by alveolar macrophages (AMs). We show AMs post-BMT overproduce granulocyte-macrophage colony-stimulating factor (GM-CSF), whereas GM-CSF in lung homogenates is impaired both at baseline and in response to infection post-BMT. Homeostatic regulation of GM-CSF may occur by hematopoietic/structural cell cross talk. To determine whether AM overproduction of GM-CSF influenced immunosuppression post-BMT, we compared mice that received BMT from wild-type donors (control BMT) or mice that rec

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13

Lieschke, GJ, E. Stanley, D. Grail, et al. "Mice lacking both macrophage- and granulocyte-macrophage colony- stimulating factor have macrophages and coexistent osteopetrosis and severe lung disease." Blood 84, no. 1 (1994): 27–35. http://dx.doi.org/10.1182/blood.v84.1.27.27.

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Abstract Mice deficient in granulocyte-macrophage colony-stimulating factor (GM- CSF) and macrophage colony-stimulating factor (M-CSF, CSF-1) were generated by interbreeding GM-CSF-deficient mice generated by gene targeting (genotype GM-/-) with M-CSF-deficient osteopetrotic mice (genotype M-/-, op/op). Mice deficient in both GM-CSF and M-CSF (genotype GM-/-M-/-) are viable and have coexistent features corresponding to mice deficient in either factor alone. Like M-CSF- deficient mice, they have osteopetrosis and are toothless because of failure of incisor eruption. Like GM-CSF-deficient mice,

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14

Lieschke, GJ, E. Stanley, D. Grail, et al. "Mice lacking both macrophage- and granulocyte-macrophage colony- stimulating factor have macrophages and coexistent osteopetrosis and severe lung disease." Blood 84, no. 1 (1994): 27–35. http://dx.doi.org/10.1182/blood.v84.1.27.bloodjournal84127.

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Mice deficient in granulocyte-macrophage colony-stimulating factor (GM- CSF) and macrophage colony-stimulating factor (M-CSF, CSF-1) were generated by interbreeding GM-CSF-deficient mice generated by gene targeting (genotype GM-/-) with M-CSF-deficient osteopetrotic mice (genotype M-/-, op/op). Mice deficient in both GM-CSF and M-CSF (genotype GM-/-M-/-) are viable and have coexistent features corresponding to mice deficient in either factor alone. Like M-CSF- deficient mice, they have osteopetrosis and are toothless because of failure of incisor eruption. Like GM-CSF-deficient mice, they have

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15

Osborne, C. S., M. A. Vadas, and P. N. Cockerill. "Transcriptional regulation of mouse granulocyte-macrophage colony-stimulating factor/IL-3 locus." Journal of Immunology 155, no. 1 (1995): 226–35. http://dx.doi.org/10.4049/jimmunol.155.1.226.

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Abstract Granulocyte-macrophage (GM)-CSF and IL-3 are hemopoietic growth factors whose genes are closely linked in both humans and mice. In humans, the GM-CSF and IL-3 genes are regulated by a cyclosporin A-inhibitable enhancer located 3 kb upstream of the GM-CSF gene that is inducible by signals that mimic TCR activation. To search for a murine homologue of this enhancer we probed mouse genomic DNA and located a 400-bp element 2 kb upstream of the mouse GM-CSF gene that was 76% homologous with the human GM-CSF enhancer. Like the human GM-CSF enhancer, this element formed a cyclosporin A-inhib

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16

Rothstein, G., SM Rhondeau, CA Peters, RD Christensen, D. Lynch, and S. Gillis. "Stimulation of neutrophil production in CSF-1-responsive clones." Blood 72, no. 3 (1988): 898–902. http://dx.doi.org/10.1182/blood.v72.3.898.898.

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Abstract The hematopoietic growth factor CSF-1 has been considered relatively lineage specific for the production of macrophages, whereas GM-CSF elicits a predominance of neutrophils. It is likely that in vivo, individual clones are stimulated by the two CSFs, although the effect of dual stimulation on progenitors and their progeny has not been completely explored. We found that in cultures initiated with low concentrations of CSF-1 or GM-CSF, alone or in combination, production of macrophages predominated. Maximally stimulatory concentrations of CSF-1 elicited a predominance of macrophages, w

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17

Rothstein, G., SM Rhondeau, CA Peters, RD Christensen, D. Lynch, and S. Gillis. "Stimulation of neutrophil production in CSF-1-responsive clones." Blood 72, no. 3 (1988): 898–902. http://dx.doi.org/10.1182/blood.v72.3.898.bloodjournal723898.

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The hematopoietic growth factor CSF-1 has been considered relatively lineage specific for the production of macrophages, whereas GM-CSF elicits a predominance of neutrophils. It is likely that in vivo, individual clones are stimulated by the two CSFs, although the effect of dual stimulation on progenitors and their progeny has not been completely explored. We found that in cultures initiated with low concentrations of CSF-1 or GM-CSF, alone or in combination, production of macrophages predominated. Maximally stimulatory concentrations of CSF-1 elicited a predominance of macrophages, whereas ma

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18

Wognum, AW, Y. Westerman, TP Visser, and G. Wagemaker. "Distribution of receptors for granulocyte-macrophage colony-stimulating factor on immature CD34+ bone marrow cells, differentiating monomyeloid progenitors, and mature blood cell subsets." Blood 84, no. 3 (1994): 764–74. http://dx.doi.org/10.1182/blood.v84.3.764.764.

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Abstract Biotin-labeled granulocyte-macrophage colony-stimulating factor (GM- CSF), in combination with phycoerythrin-conjugated streptavidin, enabled flow cytometric analysis of specific cell-surface GM-CSF receptors on rhesus monkey bone marrow (BM) and peripheral blood (PB) cells. GM-CSF receptors were readily detected on PB monocytes and neutrophils, but not on lymphocytes. In BM, GM-CSF receptors were identified on monocyte and neutrophil precursors and on subsets of cells that expressed the CD34 antigen. CD34+ cells with high GM-CSF- receptor expression coexpressed high levels of the cla

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19

Wognum, AW, Y. Westerman, TP Visser, and G. Wagemaker. "Distribution of receptors for granulocyte-macrophage colony-stimulating factor on immature CD34+ bone marrow cells, differentiating monomyeloid progenitors, and mature blood cell subsets." Blood 84, no. 3 (1994): 764–74. http://dx.doi.org/10.1182/blood.v84.3.764.bloodjournal843764.

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Biotin-labeled granulocyte-macrophage colony-stimulating factor (GM- CSF), in combination with phycoerythrin-conjugated streptavidin, enabled flow cytometric analysis of specific cell-surface GM-CSF receptors on rhesus monkey bone marrow (BM) and peripheral blood (PB) cells. GM-CSF receptors were readily detected on PB monocytes and neutrophils, but not on lymphocytes. In BM, GM-CSF receptors were identified on monocyte and neutrophil precursors and on subsets of cells that expressed the CD34 antigen. CD34+ cells with high GM-CSF- receptor expression coexpressed high levels of the class II maj

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20

Nimer, S. D., M. J. Gates, H. P. Koeffler, and J. C. Gasson. "Multiple mechanisms control the expression of granulocyte-macrophage colony-stimulating factor by human fibroblasts." Journal of Immunology 143, no. 7 (1989): 2374–77. http://dx.doi.org/10.4049/jimmunol.143.7.2374.

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Abstract Human granulocyte-macrophage colony-stimulating factor (GM-CSF) has in vitro and in vivo effects on hemopoiesis and enhances the function of circulating mature myeloid cells. Unstimulated fibroblasts show low level GM-CSF transcription but no accumulation of GM-CSF mRNA or protein, whereas fibroblasts stimulated by TNF-alpha, IL-1, and phorbol diester have been shown to produce and secrete GM-CSF. To determine the mechanisms controlling the expression of GM-CSF in human fibroblasts, we used a transient transfection assay to look at the effect of TNF-alpha, IL-1 and phorbol diester on

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21

Kanakura, Y., SA Cannistra, CB Brown, et al. "Identification of functionally distinct domains of human granulocyte- macrophage colony-stimulating factor using monoclonal antibodies." Blood 77, no. 5 (1991): 1033–43. http://dx.doi.org/10.1182/blood.v77.5.1033.1033.

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Abstract Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a glycoprotein that is required for the survival, growth, and differentiation of hematopoietic progenitor cells. Although the primary structure of GM-CSF is known from cDNA cloning, the relationship between structure and function of GM-CSF is not fully understood. Fifteen different monoclonal antibodies (MoAbs) to human GM-CSF were generated to map immunologically distinct areas of the molecule. Each of the MoAbs was biotinylated and shown by enzyme-linked immunosorbent assay to bind to recombinant GM-CSF that had been affix

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22

Kanakura, Y., SA Cannistra, CB Brown, et al. "Identification of functionally distinct domains of human granulocyte- macrophage colony-stimulating factor using monoclonal antibodies." Blood 77, no. 5 (1991): 1033–43. http://dx.doi.org/10.1182/blood.v77.5.1033.bloodjournal7751033.

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a glycoprotein that is required for the survival, growth, and differentiation of hematopoietic progenitor cells. Although the primary structure of GM-CSF is known from cDNA cloning, the relationship between structure and function of GM-CSF is not fully understood. Fifteen different monoclonal antibodies (MoAbs) to human GM-CSF were generated to map immunologically distinct areas of the molecule. Each of the MoAbs was biotinylated and shown by enzyme-linked immunosorbent assay to bind to recombinant GM-CSF that had been affixed to a s

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23

Suzuki, Takuji, Takuro Sakagami, Bruce K. Rubin, et al. "Familial pulmonary alveolar proteinosis caused by mutations in CSF2RA." Journal of Experimental Medicine 205, no. 12 (2008): 2703–10. http://dx.doi.org/10.1084/jem.20080990.

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Primary pulmonary alveolar proteinosis (PAP) is a rare syndrome characterized by accumulation of surfactant in the lungs that is presumed to be mediated by disruption of granulocyte/macrophage colony-stimulating factor (GM-CSF) signaling based on studies in genetically modified mice. The effects of GM-CSF are mediated by heterologous receptors composed of GM-CSF binding (GM-CSF-Rα) and nonbinding affinity-enhancing (GM-CSF-Rβ) subunits. We describe PAP, failure to thrive, and increased GM-CSF levels in two sisters aged 6 and 8 yr with abnormalities of both GM-CSF-Rα–encoding alleles (CSF2RA).

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24

Mehta, Hrishikesh M., Michael Malandra, and Seth J. Corey. "G-CSF and GM-CSF in Neutropenia." Journal of Immunology 195, no. 4 (2015): 1341–49. http://dx.doi.org/10.4049/jimmunol.1500861.

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25

Weisdorf, DJ, CM Verfaillie, SM Davies, et al. "Hematopoietic growth factors for graft failure after bone marrow transplantation: a randomized trial of granulocyte-macrophage colony- stimulating factor (GM-CSF) versus sequential GM-CSF plus granulocyte- CSF." Blood 85, no. 12 (1995): 3452–56. http://dx.doi.org/10.1182/blood.v85.12.3452.bloodjournal85123452.

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Delay in hematologic recovery after bone marrow transplantation (BMT) can extend and amplify the risks of infection and hemorrhage, compromise patients' survival, and increase the duration and cost of hospitalization. Because current studies suggest that granulocyte-macrophage (GM) colony-stimulating factor (CSF) may potentiate the sensitivity of hematopoietic progenitor cells to G-CSF, we performed a prospective, randomized trial comparing GM-CSF (250 micrograms/m2/d x 14 days) versus sequential GM-CSF x 7 days followed by G-CSF (5 micrograms/kg/d x 7 days) as treatment for primary or seconda

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26

Khanjari, F. "GM-CSF and proteinosis." Thorax 58, no. 7 (2003): 645. http://dx.doi.org/10.1136/thorax.58.7.645.

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27

Papatriantafyllou, Maria. "GM-CSF in focus." Nature Reviews Immunology 11, no. 6 (2011): 370–71. http://dx.doi.org/10.1038/nri2996.

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28

Gillis, Steven, and Leslie Garrison. "Antibodies to GM-CSF." Lancet 335, no. 8699 (1990): 1217. http://dx.doi.org/10.1016/0140-6736(90)92735-z.

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29

Middleton, M., and N. Thatcher. "G- and GM-CSF." International Journal of Antimicrobial Agents 10, no. 2 (1998): 91–93. http://dx.doi.org/10.1016/s0924-8579(98)00015-6.

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30

Stewart-Akers, AM, JS Cairns, DJ Tweardy, and SA McCarthy. "Granulocyte-macrophage colony-stimulating factor augmentation of T-cell receptor-dependent and T-cell receptor-independent thymocyte proliferation." Blood 83, no. 3 (1994): 713–23. http://dx.doi.org/10.1182/blood.v83.3.713.713.

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Abstract The effects of granulocyte-macrophage colony-stimulating factor (GM- CSF) are not confined to cells of the myeloid lineage. GM-CSF has been shown to have effects on mature T cells and both mature and immature T- cell lines. We therefore examined the GM-CSF responsiveness of murine thymocytes to investigate whether GM-CSF also affected normal immature T lymphocytes. The studies presented here indicate that GM-CSF augments accessory cell (AC)-dependent T-cell receptor (TCR)-mediated proliferation of unseparated thymocyte populations. To identify the GM- CSF responsive cell type, thymic

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31

Stewart-Akers, AM, JS Cairns, DJ Tweardy, and SA McCarthy. "Granulocyte-macrophage colony-stimulating factor augmentation of T-cell receptor-dependent and T-cell receptor-independent thymocyte proliferation." Blood 83, no. 3 (1994): 713–23. http://dx.doi.org/10.1182/blood.v83.3.713.bloodjournal833713.

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The effects of granulocyte-macrophage colony-stimulating factor (GM- CSF) are not confined to cells of the myeloid lineage. GM-CSF has been shown to have effects on mature T cells and both mature and immature T- cell lines. We therefore examined the GM-CSF responsiveness of murine thymocytes to investigate whether GM-CSF also affected normal immature T lymphocytes. The studies presented here indicate that GM-CSF augments accessory cell (AC)-dependent T-cell receptor (TCR)-mediated proliferation of unseparated thymocyte populations. To identify the GM- CSF responsive cell type, thymic AC and T

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32

Metcalf, Donald, Nicos A. Nicola, Sandra Mifsud, and Ladina Di Rago. "Receptor Clearance Obscures the Magnitude of Granulocyte-Macrophage Colony-Stimulating Factor Responses in Mice to Endotoxin or Local Infections." Blood 93, no. 5 (1999): 1579–85. http://dx.doi.org/10.1182/blood.v93.5.1579.

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Abstract Marrow cells from mice lacking high-affinity receptors for granulocyte-macrophage colony-stimulating factor (GM-CSF; βc−/− mice) were shown to bind and internalize much less GM-CSF than cells from normal (βc+/+) mice. βc−/− mice were used to determine the effect of negligible receptor-mediated clearance on detectible GM-CSF responses to the intravenous injection of endotoxin or the intraperitoneal injection of casein plus microorganisms. Unlike the minor serum GM-CSF responses to endotoxin seen in βc+/+ mice, serum GM-CSF levels rose 30-fold to 9 ng/mL in βc−/− mice even though loss o

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Metcalf, Donald, Nicos A. Nicola, Sandra Mifsud, and Ladina Di Rago. "Receptor Clearance Obscures the Magnitude of Granulocyte-Macrophage Colony-Stimulating Factor Responses in Mice to Endotoxin or Local Infections." Blood 93, no. 5 (1999): 1579–85. http://dx.doi.org/10.1182/blood.v93.5.1579.405k01_1579_1585.

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Marrow cells from mice lacking high-affinity receptors for granulocyte-macrophage colony-stimulating factor (GM-CSF; βc−/− mice) were shown to bind and internalize much less GM-CSF than cells from normal (βc+/+) mice. βc−/− mice were used to determine the effect of negligible receptor-mediated clearance on detectible GM-CSF responses to the intravenous injection of endotoxin or the intraperitoneal injection of casein plus microorganisms. Unlike the minor serum GM-CSF responses to endotoxin seen in βc+/+ mice, serum GM-CSF levels rose 30-fold to 9 ng/mL in βc−/− mice even though loss of GM-CSF

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34

Freedman, MH, T. Grunberger, P. Correa, AA Axelrad, ID Dube, and A. Cohen. "Autocrine and paracrine growth control by granulocyte-monocyte colony- stimulating factor of acute lymphoblastic leukemia cells." Blood 81, no. 11 (1993): 3068–75. http://dx.doi.org/10.1182/blood.v81.11.3068.3068.

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Abstract Blast colony assays were performed on freshly obtained bone marrow samples from 19 newly diagnosed or relapsed children with acute lymphoblastic leukemia (ALL) of B lineage to determine the effect of added granulocyte-monocyte colony-stimulating factor (GM-CSF). Of the 19 marrow samples tested, 7 responded to GM-CSF with a mean increase in ALL blast colonies of 346%. Blast cells from one of the responders chosen for flow cytometric study showed expression of GM-CSF receptors on 38% of cells. These findings prompted us to establish five ALL cell lines of diverse phenotypes to examine t

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35

Freedman, MH, T. Grunberger, P. Correa, AA Axelrad, ID Dube, and A. Cohen. "Autocrine and paracrine growth control by granulocyte-monocyte colony- stimulating factor of acute lymphoblastic leukemia cells." Blood 81, no. 11 (1993): 3068–75. http://dx.doi.org/10.1182/blood.v81.11.3068.bloodjournal81113068.

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Blast colony assays were performed on freshly obtained bone marrow samples from 19 newly diagnosed or relapsed children with acute lymphoblastic leukemia (ALL) of B lineage to determine the effect of added granulocyte-monocyte colony-stimulating factor (GM-CSF). Of the 19 marrow samples tested, 7 responded to GM-CSF with a mean increase in ALL blast colonies of 346%. Blast cells from one of the responders chosen for flow cytometric study showed expression of GM-CSF receptors on 38% of cells. These findings prompted us to establish five ALL cell lines of diverse phenotypes to examine the expres

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36

Berclaz, Pierre-Yves, Yoko Shibata, Jeffrey A. Whitsett та Bruce C. Trapnell. "GM-CSF, via PU.1, regulates alveolar macrophage FcγR-mediated phagocytosis and the IL-18/IFN-γ–mediated molecular connection between innate and adaptive immunity in the lung". Blood 100, № 12 (2002): 4193–200. http://dx.doi.org/10.1182/blood-2002-04-1102.

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Severely impaired pulmonary microbial clearance was observed in granulocyte-macrophage colony-stimulating factor (GM-CSF)–deficient mice. To determine mechanisms by which GM-CSF mediates lung host defense, FcγR-mediated phagocytosis (opsonophagocytosis) by alveolar macrophages (AMs) was assessed in GM-CSF–sufficient (GM+/+) and –deficient (GM−/−) mice and in GM−/− mice expressing GM-CSF only in the lungs from a surfactant protein C (SPC) promoter (SPC-GM+/+/GM−/−). Opsonophagocytosis by GM−/− AMs was severely impaired and was restored by pulmonary GM-CSF expression in vivo or by PU.1 expressio

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37

Chen, BD, CR Clark, and TH Chou. "Granulocyte/macrophage colony-stimulating factor stimulates monocyte and tissue macrophage proliferation and enhances their responsiveness to macrophage colony-stimulating factor." Blood 71, no. 4 (1988): 997–1002. http://dx.doi.org/10.1182/blood.v71.4.997.997.

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Abstract Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a specific humoral growth factor that stimulates both neutrophilic granulocyte and macrophage production by bone marrow hematopoietic progenitor cells. GM-CSF also stimulates the proliferation and clonal growth of both tissue macrophages and blood monocytes. Although at low concentrations GM-CSF was unable to support the long-term growth of tissue macrophages, it greatly enhanced their responsiveness to macrophage CSF (M-CSF, or CSF-1). This effect was also observed by treating macrophages with GM-CSF for a short time. GM-CS

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38

Chen, BD, CR Clark, and TH Chou. "Granulocyte/macrophage colony-stimulating factor stimulates monocyte and tissue macrophage proliferation and enhances their responsiveness to macrophage colony-stimulating factor." Blood 71, no. 4 (1988): 997–1002. http://dx.doi.org/10.1182/blood.v71.4.997.bloodjournal714997.

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a specific humoral growth factor that stimulates both neutrophilic granulocyte and macrophage production by bone marrow hematopoietic progenitor cells. GM-CSF also stimulates the proliferation and clonal growth of both tissue macrophages and blood monocytes. Although at low concentrations GM-CSF was unable to support the long-term growth of tissue macrophages, it greatly enhanced their responsiveness to macrophage CSF (M-CSF, or CSF-1). This effect was also observed by treating macrophages with GM-CSF for a short time. GM-CSF did not

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39

Charbeneau, Ryan P., Paul J. Christensen, Cara J. Chrisman, et al. "Impaired synthesis of prostaglandin E2 by lung fibroblasts and alveolar epithelial cells from GM-CSF−/− mice: implications for fibroproliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 6 (2003): L1103—L1111. http://dx.doi.org/10.1152/ajplung.00350.2002.

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Prostaglandin E2 (PGE2) is a potent suppressor of fibroblast activity. We previously reported that bleomycin-induced pulmonary fibrosis was exaggerated in granulocyte-macrophage colony-stimulating factor knockout (GM-CSF−/−) mice compared with wild-type (GM-CSF+/+) mice and that increased fibrosis was associated with decreased PGE2 levels in lung homogenates and alveolar macrophage cultures. Pulmonary fibroblasts and alveolar epithelial cells (AECs) represent additional cellular sources of PGE2 within the lung. Therefore, we examined fibroblasts and AECs from GM-CSF−/− mice, and we found that

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Kassem, Neemat M., Alya M. Ayad, Noha M. El Husseiny, Doaa M. El-Demerdash, Hebatallah A. Kassem, and Mervat M. Mattar. "Role of Granulocyte-Macrophage Colony-Stimulating Factor in Acute Myeloid Leukemia/Myelodysplastic Syndromes." Journal of Global Oncology, no. 4 (December 2018): 1–6. http://dx.doi.org/10.1200/jgo.2017.009332.

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Purpose Granulocyte-macrophage colony-stimulating factor (GM-CSF) cytokine stimulates growth, differentiation, and function of myeloid progenitors. We aimed to study the role of GM-CSF gene expression, its protein, and antibodies in patients with acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) and their correlation to disease behavior and treatment outcome. The study included 50 Egyptian patients with AML/MDS in addition to 20 healthy volunteers as control subjects. Patients and Methods Assessment of GM-CSF gene expression was performed by quantitative real-time polymerase chain rea

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Chen, T. T., and R. Levy. "Induction of autoantibody responses to GM-CSF by hyperimmunization with an Id-GM-CSF fusion protein." Journal of Immunology 154, no. 7 (1995): 3105–17. http://dx.doi.org/10.4049/jimmunol.154.7.3105.

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Abstract Fusion proteins consisting of an Ig containing xenogenic constant regions and granulocyte-macrophage colony stimulating factor (Id-GM-CSF) are potent immunogens capable of inducing anti-idiotypic Abs after two immunizations, without the usual need for adjuvants or carrier proteins. In this study, we investigated the effects of hyperimmunization with Id-GM-CSF and found that it induces anti-GM-CSF Abs that could bind to GM-CSF and neutralize its bioactivity in vitro. However, no detrimental effects of the anti-GM-CSF activity were apparent on the general health of the animals or on the

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Nakata, K., K. S. Akagawa, M. Fukayama, Y. Hayashi, M. Kadokura, and T. Tokunaga. "Granulocyte-macrophage colony-stimulating factor promotes the proliferation of human alveolar macrophages in vitro." Journal of Immunology 147, no. 4 (1991): 1266–72. http://dx.doi.org/10.4049/jimmunol.147.4.1266.

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Abstract The effects of granulocyte-macrophage (GM-CSF) or macrophage-CSF on in vitro proliferation of human alveolar macrophages (AM) were evaluated. AM of healthy volunteers incubated with recombinant human GM-CSF revealed incorporation of [3H]thymidine in vitro. The maximum incorporation was observed at 20 U/ml of GM-CSF on day 3. The proportion of proliferating cells incubated with 20 U/ml of GM-CSF from day 3 to day 4 was 8 to 11% of the total, whereas 3 to 5% of cells proliferated without GM-CSF. The number of cell nuclei increased 1.30- to 1.68-fold in the initial 7 days during incubati

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Kitching, A. Richard, Xiao Ru Huang, Amanda L. Turner, Peter G. Tipping, Ashley R. Dunn, and Stephen R. Holdsworth. "The Requirement for Granulocyte-Macrophage Colony-Stimulating Factor and Granulocyte Colony-Stimulating Factor in Leukocyte-Mediated Immune Glomerular Injury." Journal of the American Society of Nephrology 13, no. 2 (2002): 350–58. http://dx.doi.org/10.1681/asn.v132350.

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ABSTRACT. Proliferative glomerulonephritis in humans is characterized by the presence of leukocytes in glomeruli. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) can potentially stimulate or affect T cell, macrophage, and neutrophil function. To define the roles of GM-CSF and G-CSF in leukocyte-mediated glomerulonephritis, glomerular injury was studied in mice genetically deficient in either GM-CSF (GM-CSF −/− mice) or G-CSF (G-CSF −/− mice). Two models of glomerulonephritis were studied: neutrophil-mediated heterologous-phase anti-gl

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Brown, CB, P. Beaudry, TD Laing, S. Shoemaker, and K. Kaushansky. "In vitro characterization of the human recombinant soluble granulocyte- macrophage colony-stimulating factor receptor." Blood 85, no. 6 (1995): 1488–95. http://dx.doi.org/10.1182/blood.v85.6.1488.bloodjournal8561488.

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We have cloned, expressed, and partially purified a naturally occurring, truncated, soluble form of the human granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor alpha subunit to investigate its biochemical and biologic properties. The soluble receptor species lacks the transmembrane and cytoplasmic domains that are presumably removed from the intact receptor cDNA by a mechanism of alternative splicing. The resulting soluble 55- to 60-kD glycosylated receptor species binds GM-CSF with a dissociation constant (kd) of 3.8 nmol/L. The soluble GM-CSF receptor successfully competes f

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Ni, Keping, and Helen C. O'Neill. "Development of Dendritic Cells from GM-CSF-/-Miceinvitro: GM-CSF Enhances Production and Survival of Cells." Developmental Immunology 8, no. 2 (2001): 133–46. http://dx.doi.org/10.1155/2001/68024.

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The production of dendritic cells (DC) from haemopoietic progenitors maintained in long term stroma-dependent cultures (LTC) of spleen or bone marrow (BM) occurs independently of added granulocyte/macrophage colony stimulating factor (GM-CSF). The possibility that cultures depend on endogenous GM-CSF produced in low levels was tested by attempting to generate LTC from spleen and BM of GM-CSF-/-mice. Multiple cultures from GM-CSF-/-and wild type mice were established and compared for cell production. GM-CSF-/-LTC developed more slowly, but by 16 weeks produced cells resembling DC in numbers com

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Urashima, Mitsuyoshi, Gerrard Teoh, Dharminder Chauhan, et al. "MDM2 Protein Overexpression Inhibits Apoptosis of TF-1 Granulocyte-Macrophage Colony-Stimulating Factor–Dependent Acute Myeloblastic Leukemia Cells." Blood 92, no. 3 (1998): 959–67. http://dx.doi.org/10.1182/blood.v92.3.959.414k21_959_967.

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a growth factor for acute myeloblastic leukemia (AML) cells. Murine double minute 2 (MDM2) oncoprotein, a potent inhibitor of wild-type p53 (wtp53), can function both to induce cell proliferation and enhance cell survival, and is frequently overexpressed in leukemias. Therefore, we focused on the importance of MDM2 protein in GM-CSF–dependent versus GM-CSF– independent growth of AML cells. The TF-1 AML cell line, which has both wtp53 and mutant p53 genes, showed GM-CSF–dependent growth; deprivation of GM-CSF resulted in G1 growth arr

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Patel, Snehal, David McWilliams, Christine T. Fischette, Jaye Thompson, Mira Patel, and F. Joseph Daugherty. "Final five-year median follow-up safety data from a prospective, randomized, placebo-controlled, single-blinded, multicenter, phase IIb study evaluating the use of HER2/neu peptide GP2 + GM-CSF vs. GM-CSF alone after adjuvant trastuzumab in HER2-positive women with operable breast cancer." Journal of Clinical Oncology 39, no. 15_suppl (2021): 542. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.542.

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542 Background: The final analysis of the GP2 prospective, randomized, placebo-controlled, single-blinded, multicenter Phase IIb trial investigating GP2+GM-CSF administered in the adjuvant setting to node-positive and high-risk node-negative breast cancer patients with tumors expressing any degree of HER2 (immuno-histochemistry [IHC] 1-3+) ( NCT00524277) is now complete with 5 year follow-up. The trial enrolled HLA-A02 patients randomized to receive GP2+GM-CSF versus GM-CSF alone. It was previously reported that completion of the GP2+GM-CSF Primary Immunization Series (PIS) reduced recurrence

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Kreitman, Robert J., and Ira Pastan. "Recombinant Toxins Containing Human Granulocyte-Macrophage Colony-Stimulating Factor and Either Pseudomonas Exotoxin or Diphtheria Toxin Kill Gastrointestinal Cancer and Leukemia Cells." Blood 90, no. 1 (1997): 252–59. http://dx.doi.org/10.1182/blood.v90.1.252.

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Abstract The granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) is a potential target for toxin-directed therapy, because it is overexpressed on many leukemias and solid tumors and apparently not on stem cells. To investigate the potential therapeutic use of GM-CSF toxins, we fused human GM-CSF to truncated forms of either Pseudomonas exotoxin (PE) or diphtheria toxin (DT) and tested the cytotoxicity of the resulting GM-CSF–PE38KDEL and DT388–GM-CSF on human gastrointestinal (GI) carcinomas and leukemias. Toward gastric and colon cancer cell lines, GM-CSF–PE38KDEL was much mor

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Kreitman, Robert J., and Ira Pastan. "Recombinant Toxins Containing Human Granulocyte-Macrophage Colony-Stimulating Factor and Either Pseudomonas Exotoxin or Diphtheria Toxin Kill Gastrointestinal Cancer and Leukemia Cells." Blood 90, no. 1 (1997): 252–59. http://dx.doi.org/10.1182/blood.v90.1.252.252_252_259.

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The granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) is a potential target for toxin-directed therapy, because it is overexpressed on many leukemias and solid tumors and apparently not on stem cells. To investigate the potential therapeutic use of GM-CSF toxins, we fused human GM-CSF to truncated forms of either Pseudomonas exotoxin (PE) or diphtheria toxin (DT) and tested the cytotoxicity of the resulting GM-CSF–PE38KDEL and DT388–GM-CSF on human gastrointestinal (GI) carcinomas and leukemias. Toward gastric and colon cancer cell lines, GM-CSF–PE38KDEL was much more cytotox

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Fan, K., Q. Ruan, L. Sensenbrenner, and B. D. Chen. "Up-regulation of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptors in murine peritoneal exudate macrophages by both GM-CSF and IL-3." Journal of Immunology 149, no. 1 (1992): 96–102. http://dx.doi.org/10.4049/jimmunol.149.1.96.

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Abstract Murine peritoneal exudate macrophages (PEM) display multiple CSF receptors. In this study, the expression of granulocyte-macrophage (GM)-CSF receptors in PEM was studied. PEM displayed over 5000 single type, high affinity GM-CSF receptors/cell with a Kd = 38 to 42 pM and an apparent molecular mass of 86,000 Da. Treatment of PEM with low, but not high, concentrations of recombinant murine (rMu) GM-CSF continuously for 24 h resulted in a marked up-regulation of GM-CSF receptors in PEM. A similar up-regulation of GM-CSF receptors also was detected in PEM cultures treated with rMuIL-3 (1-

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