Source:http://linkedlifedata.com/resource/pubmed/id/10843759
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2000-8-23
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pubmed:abstractText |
Since some cytokines effectively enhance the cytotoxicity of monoclonal antibodies, we investigated whether a combination of cytokines can augment the antibody-dependent cellular cytotoxicity (ADCC) of monoclonal antibodies 17-1A and BR55-2 against the colorectal carcinoma cell line HT29. Since monocytes/macrophages are important effector cells for ADCC, we used a new flow cytometric cytotoxicity assay, which allows the analysis of long-term-ADCC exerted by these cells. In our previous studies with peripheral blood mononuclear cells from normal donors, we found that IL-2, IL-12 and IFN-alpha increase ADCC. Therefore, we examined whether combination of these three cytokines with IL-2, IL-4, IL-6, IL-10, IL-12, IFN-alpha, IFN-gamma, GM-CSF, M-CSF and TNF-alpha may yield higher ADCC than obtained by the application of single cytokines. Indeed, we found that the combinations IL-2/IFN-alpha, IL-2/IL-12 and IL-12/IFN-alpha potentiated ADCC. Interestingly, the ineffective single cytokines TNF-alpha and GM-CSF in the combinations IL-2/TNF-alpha, IFN-alpha/TNF-alpha and IFN-alpha/GM-CSF also proved to enhance ADCC. In contrast, IL-4 significantly suppressed the IL-2, IL-12 and IFN-alpha-induced ADCC. In addition, the immunosuppressive cytokine IL-10 in higher concentrations significantly suppressed the IL-12-induced-ADCC. Our results may be useful to find combinations of cytokines and mAb for the treatment of cancer.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1043-4666
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2000 Academic Press.
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
756-61
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:10843759-Antibodies, Monoclonal,
pubmed-meshheading:10843759-Antibody-Dependent Cell Cytotoxicity,
pubmed-meshheading:10843759-Colonic Neoplasms,
pubmed-meshheading:10843759-Cytotoxicity, Immunologic,
pubmed-meshheading:10843759-Humans,
pubmed-meshheading:10843759-Interferon Type I,
pubmed-meshheading:10843759-Interleukin-12,
pubmed-meshheading:10843759-Interleukin-2,
pubmed-meshheading:10843759-Interleukin-4,
pubmed-meshheading:10843759-Recombinant Proteins,
pubmed-meshheading:10843759-Tumor Cells, Cultured
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pubmed:year |
2000
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pubmed:articleTitle |
Combinations of the cytokines IL-12, IL-2 and IFN-alpha significantly augment whereas the cytokine IL-4 suppresses the cytokine-induced antibody-dependent cellular cytotoxicity of monoclonal antibodies 17-1A and BR55-2.
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pubmed:affiliation |
Medizinische Klinik und Poliklinik I, Allgemeine Innere Medizin, Universität Bonn, Bonn, Germany. Flieger@uni-bonn.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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