Effect of granulocyte‐macrophage colony‐stimulating factor treatment on phenotype, cytokine release and cytotoxicity of circulating blood monocytes and monocyte‐derived macrophages

Hennemann, B.; Kreutz, Marina; Rehm, Annegret; Andreesen, Reinhard

doi:10.1046/j.1365-2141.1998.00922.x

Cited by 20 publications

(12 citation statements)

References 27 publications

(43 reference statements)

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“…The priming of TNF␣ production by GM-CSF has been well documented (20). Although enhanced LPS-induced IL-10 synthesis after GM-CSF in vitro incubation has been found in human monocytes (13), Hartung et al (21) found no change in stimulated or unstimulated IL-10 synthesis in donors treated with GM-CSF, and Hennemann et al (22) reported that GM-CSF in cancer patients decreased IL-10 formation and that enhanced TNF␣ synthesis of LPSstimulated blood cultures. Different in vitro and in vivo effects can be explained by generation of a novel monocyte population after in vivo treatment with GM-CSF, a phenomena described after GM-CSF therapy (20,22).…”

Section: Discussionmentioning

confidence: 95%

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Effect of granulocyte-macrophage colony-stimulating factor on the immune response of circulating monocytes after severe trauma

Flohé

Lendemans

Selbach

et al. 2003

Critical Care Medicine

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Section: Discussionmentioning

confidence: 95%

“…Hence, GM-CSF treatment results in elevated TNF␣, IL-1␤, and IL-6 in response to LPS stimulation in vitro and in vivo (13,20), whereas the results for interferon-␥, IL-1Ra, and IL-10 are inconsistent. Studies have shown both increased (13,21) and decreased (22) synthesis of the latter on ex vivo LPS stimulation.…”

mentioning

confidence: 97%

Effect of granulocyte-macrophage colony-stimulating factor on the immune response of circulating monocytes after severe trauma

Flohé

Lendemans

Selbach

et al. 2003

Critical Care Medicine

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“…GM-CSF enhances neutrophil chemotaxis by increasing diacylglycerol generation, enhances phagocytosis by increasing FcR III expression, and enhances killing via increasing O 2 Ϫ generation and cytokine release (12,23,29,53). Therefore, combinations of GM-CSF with antifungal agents in fungal infections appear to be reasonable.…”

Section: Discussionmentioning

confidence: 99%

Lactoferrin Peptide Increases the Survival of Candida albicans - Inoculated Mice by Upregulating Neutrophil and Macrophage Functions, Especially in Combination with Amphotericin B and Granulocyte-Macrophage Colony-Stimulating Factor

et al. 2001

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To develop a new strategy to control candidiasis, we examined in vivo the anticandidal effects of a synthetic lactoferrin peptide, FKCRRWQWRM (peptide 2) and the peptide that mimics it, FKARRWQWRM (peptide 2). Although all mice that underwent intraperitoneal injection of 5 ؋ 10 8 Candida cells with or without peptide 2 died within 8 or 7 days, respectively, the survival times of mice treated with 5 to 100 g of intravenous peptide 2 per day for 5 days after the candidal inoculation were prolonged between 8.4 ؎ 2.9 and 22.4 ؎ 3.6 days, depending on the dose of peptide 2. The prolongation of survival by peptide 2 was also observed in mice that were infected with 1.0 ؋ 10 9 Candida albicans cells (3.2 ؎ 1.3 days in control mice versus 8.2 ؎ 2.4 days in the mice injected with 10 g of peptide 2 per day). In the high-dose inoculation, a combination of peptide 2 (10 g/day) with amphotericin B (0.1 g/day) and granulocyte-macrophage colony-stimulating factor (GM-CSF) (0.1 g/day) brought prolonged survival. With a combination of these agents, 60% of the mice were alive for more than 22 days. Correspondingly, peptide 2 activated phagocytes inducing inducible NO synthase and the expression of p47 phox and p67 phox , and peptide 2 increased phagocyte Candida-killing activities up to 1.5-fold of the control levels upregulating the generation of superoxide, lactoferrin, and defensin from neutrophils and macrophages. These findings indicated that the anticandidal effects of peptide 2 depend not only on the direct Candida cell growth-inhibitory activity, but also on the phagocytes' upregulatory activity, and that combinations of peptide 2 with GM-CSF and antifungal drugs will help in the development of new strategies for control of candidiasis.

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“…In addition directing GM-CSF to the tumor microenvironment using anti-HER2/neu IgG3-(GM-CSF) may lead to enhanced macrophage activation at the site of the tumor; in murine models, activated macrophages given locally and i.v. inhibit tumor growth and decrease metastatic development (54).…”

Section: Discussionmentioning

confidence: 99%

Recombinant Anti-Human HER2/neuIgG3-(GM-CSF) Fusion Protein Retains Antigen Specificity and Cytokine Function and Demonstrates Antitumor Activity

Cruz

Trinh

Morrison

et al. 2000

The Journal of Immunology

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Anti-HER2/neu therapy of human HER2/neu-expressing malignancies such as breast cancer has shown only partial success in clinical trials. To expand the clinical potential of this approach, we have genetically engineered an anti-HER2/neu IgG3 fusion protein containing GM-CSF. Anti-HER2/neu IgG3-(GM-CSF) expressed in myeloma cells was correctly assembled and secreted. It was able to target HER2/neu-expressing cells and to support growth of a GM-CSF-dependent murine myeloid cell line, FDC-P1. The Ab fusion protein activated J774.2 macrophage cells so that they exhibit an enhanced cytotoxic activity and was comparable to the parental Ab in its ability to effect Ab-dependent cellular cytotoxicity-mediated tumor cell lysis. Pharmacokinetic studies showed that anti-HER2/neu IgG3-(GM-CSF) is stable in the blood. Interestingly, the half-life of anti-HER2/neu IgG3-(GM-CSF) depended on the injected dose with longer in vivo persistence observed at higher doses. Biodistribution studies showed that anti-HER2/neu IgG3-(GM-CSF) is mainly localized in the spleen. In addition, anti-HER2/neu IgG3-(GM-CSF) was able to target the HER2/neu-expressing murine tumor CT26-HER2/neu and enhance the immune response against the targeted Ag HER2/neu. Anti-HER2/neu IgG3-(GM-CSF) is able to enhance both Th1- and Th2-mediated immune responses and treatment with this Ab fusion protein resulted in significant retardation in the growth of s.c. CT26-HER2/neu tumors. Our results suggest that anti-HER2/neu IgG3-(GM-CSF) fusion protein is useful in the treatment of HER2/neu-expressing tumors.

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Effect of granulocyte‐macrophage colony‐stimulating factor treatment on phenotype, cytokine release and cytotoxicity of circulating blood monocytes and monocyte‐derived macrophages

Cited by 20 publications

References 27 publications

Effect of granulocyte-macrophage colony-stimulating factor on the immune response of circulating monocytes after severe trauma

Effect of granulocyte-macrophage colony-stimulating factor on the immune response of circulating monocytes after severe trauma

Lactoferrin Peptide Increases the Survival of Candida albicans - Inoculated Mice by Upregulating Neutrophil and Macrophage Functions, Especially in Combination with Amphotericin B and Granulocyte-Macrophage Colony-Stimulating Factor

Recombinant Anti-Human HER2/neuIgG3-(GM-CSF) Fusion Protein Retains Antigen Specificity and Cytokine Function and Demonstrates Antitumor Activity

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