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rdf:type | |
lifeskim:mentions |
umls-concept:C0021747,
umls-concept:C0024432,
umls-concept:C0030054,
umls-concept:C0034805,
umls-concept:C0079411,
umls-concept:C0086418,
umls-concept:C0205332,
umls-concept:C0232478,
umls-concept:C0392756,
umls-concept:C0870432,
umls-concept:C0870883,
umls-concept:C1536403,
umls-concept:C1555465,
umls-concept:C1705417,
umls-concept:C2349975
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pubmed:issue |
2
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pubmed:dateCreated |
1989-4-27
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pubmed:abstractText |
Human monocyte-derived macrophages treated with recombinant IFN-gamma (rIFN-gamma) and control cells were assessed for three distinct effector functions, all mediated by Fc receptors. rIFN-gamma-primed macrophage displayed markedly reduced phagocytosis of IgG antibody-coated erythrocytes. In contrast, antibody-dependent cytotoxicity towards IgG-antibody-coated erythrocytes and IgG-antibody-coated erythrocyte-induced generation of reactive oxygen metabolite production were increased. The decreased phagocytosis was observed microscopically, as well as in a spectrometric and a radiometric phagocytosis assay. Evidence is presented that the observed impairment in phagocytosis is not the result of increased extracellular lysis or intracellular catabolism of IgG-antibody-coated erythrocytes and that it is not observed with particles ingested in an Fc receptor-independent manner. Enhanced production of reactive oxygen metabolites was detected most clearly by measurement of luminol-dependent chemiluminescence. Antibody-dependent cellular cytotoxicity was shown to proceed also under conditions impeding phagocytosis, and rIFN-gamma-treated macrophage exerted enhanced antibody-dependent cellular cytotoxicity under these conditions too. In all three assays, functional alterations were optimally expressed after a treatment with 500 U/ml for 46 hr. Analysis at the single-cell level revealed that the IFN-gamma-induced alterations were expressed by all macrophages and not the property of distinct macrophage subpopulations. This and earlier studies suggest that the modulation of Fc receptor-mediated macrophage effector functions by IFN-gamma is in part a post-receptor-binding event.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0198-8859
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
77-93
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:2494137-Antibody-Dependent Cell Cytotoxicity,
pubmed-meshheading:2494137-Cytotoxicity, Immunologic,
pubmed-meshheading:2494137-Humans,
pubmed-meshheading:2494137-Interferon-gamma,
pubmed-meshheading:2494137-Luminescent Measurements,
pubmed-meshheading:2494137-Macrophage Activation,
pubmed-meshheading:2494137-Macrophages,
pubmed-meshheading:2494137-Oxidation-Reduction,
pubmed-meshheading:2494137-Oxygen,
pubmed-meshheading:2494137-Phagocytosis,
pubmed-meshheading:2494137-Receptors, Fc,
pubmed-meshheading:2494137-Recombinant Proteins,
pubmed-meshheading:2494137-Rosette Formation
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pubmed:year |
1989
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pubmed:articleTitle |
Interferon gamma-treated human macrophages display enhanced cytolysis and generation of reactive oxygen metabolites but reduced ingestion upon Fc receptor triggering.
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pubmed:affiliation |
Institute of Veterinary Virology, University of Berne, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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