Soluble Cytostatic Factor(s) Released from Human Monocytes

Hammestrøm, J

doi:10.1111/j.1365-3083.1982.tb00654.x

Cited by 33 publications

(4 citation statements)

References 23 publications

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“…This sequence agrees with that reported for activation of human monocytes by r-IFN-7 and endotoxins [22,36]. Our demonstration that human monocytes can respond to activation stimuli such as MDP and r-IFN-'/and release a cytolytic factor to tumor cells is consistent with obersvations of others [4,5,13,29,34,48,49]. Previous studies from our laboratories have shown that the TCF activity was not abolished by the presence of serum in the medium or by treatment with protease inhibitors [49].…”

Section: Discussionsupporting

confidence: 94%

Potentiation of direct antitumor cytotoxicity and production of tumor cytolytic factors in human blood monocytes by human recombinant interferon-gamma and muramyl dipeptide derivatives

Sone

López-Berestein

Fidler

1986

Cancer Immunol Immunother

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We investigated whether human peripheral blood monocytes isolated by centrifugal elutriation from healthy donors could be activated to become tumoricidal and release tumor cytolytic factor (TCF) subsequent to incubation with recombinant human interferon-gamma (r-IFN-gamma) or a derivative of muramyl dipeptide (nor-MDP), or both. Blood monocytes incubated in endotoxin-free medium containing up to 1000 U/ml of r-IFN-gamma or in medium containing less than 1 microgram/ml of nor MDP were not activated to lyse radiolabeled allogeneic human tumor cells. In contrast, the incubation of monocytes with various dose combinations of r-IFN-gamma and nor-MDP generated significant direct cytotoxic activity as well as production of TCF. Preincubation of the r-IFN-gamma and nor-MDP mixture with polymyxin B did not inhibit the synergism, thus ruling out the possibility that the process was due to endotoxin contamination. TCF harvested from monocyte culture supernatants was cytolytic against five allogeneic tumor targets, but not against a nontumorigenic cell line. Collectively, the data demonstrate that r-IFN-gamma can prime human blood monocytes to allow their activation by synthetic nor-MDP.

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Section: Discussionsupporting

confidence: 94%

Potentiation of direct antitumor cytotoxicity and production of tumor cytolytic factors in human blood monocytes by human recombinant interferon-gamma and muramyl dipeptide derivatives

Sone

López-Berestein

Fidler

1986

Cancer Immunol Immunother

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“…These cells have a higher activity of a tyrosine-specific protein kinase as well as an increased capacity to release arachidonic acid (8,9). Previous work from this laboratory has shown that the growth of U937 cells (a histiocytic leukemia cell line) can be inhibited by purified lipomodulin (29).…”

Section: Discussionmentioning

confidence: 99%

“…Demonstration of substrates with known functions is essential to understanding the mechanisms of cellular transformation, mediated by a tyrosine-specific kinase(s). Cells that are stimulated with mitogens such as platelet-derived factor or insulin, or cells that are transformed by tumor viruses, produce larger amounts of prostaglandins, probably by increased activity of phospholipase(s) in these cells (8,9). Since activity of phospholipase(s) in neutrophils is dependent on the phosphorylation of lipomodulin, a phospholipase inhibitory protein (10), we searched for kinases that phosphorylate lipomodulin in mitogen-stimulated cells.…”

mentioning

confidence: 99%

Phosphorylation at a tyrosine residue of lipomodulin in mitogen-stimulated murine thymocytes.

Hirata

Matsuda

Notsu

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

125

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When murine thymocytes were stimulated by mitogens such as concanavalin A, the Ca2+ ionophore A23187, or 4j-phorbol 12-myristate 13-acetate, there was a marked increase of 32p incorporation into immunoprecipitable lipomodulin, a phospholipase inhibitory protein. These compounds enhanced 45Ca21 influx into thymocytes, which, in turn, increased protein phosphorylation, probably by Ca2+-and phospholipid-dependent protein kinase (protein kinase C). Cyclic 8-bromo-AMP, an inhibitor of lymphocyte mitogenesis, blocked the mitogen-stimulated phosphorylation of lipomodulin, although it stimulated the protein phosphorylation via cyclic AMP-dependent kinase (protein kinase A). On electrophoresis, the hydrolysates of 35P-labeled lipomodulin showed a single radioactive spot, which comigrated with authentic phosphotyrosine. The partially purified middle-sized tumor antigen was able to phosphorylate lipomodulin after being phosphorylated by protein kinase C but not by the catalytic subunit of protein kinase A. Our findings suggest that the activity of a tyrosine-specific kinase, which phosphorylates lipomodulin in vivo as well as in vitro, is stimulated by protein kinase C and inhibited by protein kinase A.

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“…Production of TNF is highest after 6 h of stimulation with LPS [32, 35]. This was the rationale for selecting 6 and 24 h as the stimulation times before analysis of TNF and IL-12 p40, respectively.…”

Section: Resultsmentioning

confidence: 99%

Reduction of IL-12 p40 Production in Activated Monocytes after Exposure to Diesel Exhaust Particles

Nilsen

Hagemann²,

Eikås³

et al. 2003

Int Arch Allergy Immunol

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Background: A reduction of IL-12 production by lung macrophages may partly explain the presumed adjuvant effect of diesel exhaust particles (DEP) in allergy and asthma. IL-12 stimulates T helper type 1 (Th1) lymphocytes, which inhibit Th2 cells via Th1-specific cytokines. The aim of this study was to investigate the influence of DEP on the production of IL-12 p40 in lipopolysaccharide (LPS)-activated monocytes. Methods: The human monocytic cell line Mono-Mac-6 was stimulated with LPS (200 ng/ml) and grown with DEP (0–200 µg/ml) for 0, 6 or 24 h. IL-12 p40 and the pro-inflammatory cytokine TNF were analysed in the cell supernatants by ELISA and a cell assay, respectively. Results: Levels of IL-12 p40 correlated inversely with the DEP exposure concentrations, whereas TNF increased in parallel to the DEP concentrations. At a DEP concentration of 200 µg/ml, the amount of IL-12 p40 was 35% of that observed without DEP. The corresponding TNF value was 230% of the control. Reduced viability, binding of cytokines to DEP or endotoxin in the DEP samples cannot fully explain the changes in the concentrations of these two cytokines. Conclusion: DEP seem to inhibit the production of IL-12 p40 and stimulate that of TNF in activated monocytes. This may partly explain the presumed adjuvant effect of DEP in atopy; by altering the Th1/Th2 balance via down-regulation of IL-12, the Th2 response characteristic of allergy and asthma may be favoured.

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Soluble Cytostatic Factor(s) Released from Human Monocytes

Cited by 33 publications

References 23 publications

Potentiation of direct antitumor cytotoxicity and production of tumor cytolytic factors in human blood monocytes by human recombinant interferon-gamma and muramyl dipeptide derivatives

Potentiation of direct antitumor cytotoxicity and production of tumor cytolytic factors in human blood monocytes by human recombinant interferon-gamma and muramyl dipeptide derivatives

Phosphorylation at a tyrosine residue of lipomodulin in mitogen-stimulated murine thymocytes.

Reduction of IL-12 p40 Production in Activated Monocytes after Exposure to Diesel Exhaust Particles

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