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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1994-11-16
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pubmed:abstractText |
Earlier studies from our laboratory have demonstrated that phenothiazine derivatives are capable of inhibiting mitogen-induced activation of human T-cells and thymocytes. Similar to cyclosporin A, phenothiazine derivatives exert these inhibitory effects by decreasing the accumulation of lymphokine-specific mRNA. However, proliferation of T-cell blasts and of unfractionated human thymocytes can also be induced by interleukin 2. Since activation of T-cells via the interleukin 2 receptor seems to be resistant to the action of cyclosporin A, the present study was designed to investigate whether lymphokine-induced activation could be inhibited by phenothiazine derivatives. The effects of the phenothiazine derivatives chlorpromazine and/or fluphenazine have been studied and compared to the action of cyclosporin A and FK506 in human thymocytes, human T-cell blasts and in the human T-cell line H33-HJ JA1, which is an interleukin 2 producing cell line derived from Jurkat cells. As evidenced by the incorporation of [3H]-thymidine, cyclosporin A (1 microgram/ml) and FK506 (100 ng/ml) have no or only marginal inhibitory capacity on interleukin 2-induced proliferation in all T-cell systems tested. By contrast, phenothiazine derivatives (fluphenazine > chlorpromazine) exert a dose-dependent inhibition of the activation of these cells in pharmacologically relevant micromolar concentrations. Similar results were obtained by measuring the production of interferon-gamma in the supernatants of interleukin 2-induced human thymocytes. Our results suggest that the use of phenothiazines might be helpful in immunosuppressive regimens.
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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/Chlorpromazine,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Fluphenazine,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tacrolimus
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0028-1298
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
350
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
100-3
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:7523957-Cell Division,
pubmed-meshheading:7523957-Cell Line,
pubmed-meshheading:7523957-Cells, Cultured,
pubmed-meshheading:7523957-Chlorpromazine,
pubmed-meshheading:7523957-Cyclosporine,
pubmed-meshheading:7523957-Fluphenazine,
pubmed-meshheading:7523957-Humans,
pubmed-meshheading:7523957-Interleukin-2,
pubmed-meshheading:7523957-Lymphocyte Activation,
pubmed-meshheading:7523957-Receptors, Interleukin,
pubmed-meshheading:7523957-Receptors, Interleukin-2,
pubmed-meshheading:7523957-Signal Transduction,
pubmed-meshheading:7523957-T-Lymphocytes,
pubmed-meshheading:7523957-Tacrolimus
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pubmed:year |
1994
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pubmed:articleTitle |
Inhibition of cyclosporin A/FK506 resistant, lymphokine-induced T-cell activation by phenothiazine derivatives.
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pubmed:affiliation |
Medizinische Klinik III, Universitätsklinikum Grosshadern, München, Germany.
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pubmed:publicationType |
Journal Article
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