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Inhibitors of IL-2 production and IL-2 receptor expression in human leukemic T-cell line, Jurkat
Authors:T Koizumi  Y Nakao  T Matsui  Y Katakami  N Katakami  T Fujita
Affiliation:1. Division of Hematology, Duke University Medical Center, Durham, North Carolina, USA;2. Children''s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA;3. Department of Pathology and Laboratory Medicine and Medicine, Perelman University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA;4. Department of Microbial Pathogenesis & Immunology, Texas A&M University, College Station, Texas, USA;5. Department of Microbiology & Immunology, East Carolina University, Greenville, North Carolina, USA;1. Department of Cell and Molecular Biology, Pontificia Universidad Católica de Chile, Santiago, Chile;2. CARE UC Pontificia Universidad Católica de Chile, Santiago, Chile;3. Departamento de Gastroenterología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile;4. National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD 20850, USA;5. Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA;6. FONDAP Center for Genome Regulation (CGR), Santiago, Chile
Abstract:1-(5-Isoquinolinylsulfonyl)-2-methylpiperazine (H-7), a protein kinase inhibitor, suppressed interleukin 2 (IL-2) production and IL-2 receptor (IL-2R) expression of the human leukemic T-cell line, Jurkat, induced by 12-O-tetradecanoyl-phorbol-13-acetate and phytohemagglutinin-P. This effect was significant at 5 microM H-7 without loss of cell viability. Such activity was not observed with N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA 1004), a potent inhibitor of cGMP- and cAMP-dependent kinases, and a weak inhibitor of Ca2+-phospholipid-dependent protein kinase (protein kinase C). These findings suggest that protein kinase C is more closely associated with IL-2 receptor expression and IL-2 production of T cells than cGMP- or cAMP-dependent kinases. In addition, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), a calmodulin inhibitor, suppressed both IL-2 production and IL-2R expression. Cycrosporin A (Cy A), a potent immunosuppressive drug, markedly inhibited IL-2 production of Jurkat cells whereas it did not affect the IL-2R expression. Thus, the mechanism of action of Cy A appears to differ from that of the protein kinase inhibitor, H-7, and the calmodulin inhibitor, W-7.
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