sodium-dodecyl-sulfate and Leukemia--T-Cell
sodium-dodecyl-sulfate has been researched along with Leukemia--T-Cell* in 2 studies
Other Studies
2 other study(ies) available for sodium-dodecyl-sulfate and Leukemia--T-Cell
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Bispecific humanized anti-IL-2 receptor alpha beta antibodies inhibitory for both IL-2- and IL-15-mediated proliferation.
Humanized anti-Tac (HAT) and Mik beta1 (HuMik beta 1) Abs directed at IL-2R alpha and IL-2R beta, respectively, inhibit IL-2 binding and biological activity and together act synergistically in vitro. The Abs have been used successfully in primate models of allograft rejection, graft-vs-host disease, and autoimmunity. We produced bifunctional humanized anti-IL-2R alpha beta Abs (BF-IgG) to combine the specificity of the two Abs into one entity by fusing HAT-producing NSO cells and HuMik beta 1-producing Sp2/0 cells. BF-IgG was purified using protein G-Sepharose affinity chromatography, followed by IL-2R alpha and IL-2R beta affinity chromatography and hydrophobic interaction chromatography. BF-IgG exhibited both anti-IL-2R alpha and anti-IL-2R beta specificities in binding assays. While the Ab binds the IL-2R with intermediate affinity (Kd = 2.82 nM), it does not inhibit IL-15 binding to its high affinity IL-15R. In Kit225/K6 (IL-2R alpha beta gamma+) cells, BF-IgG was 10-fold more potent than a HAT/HuMik beta 1 equimolar mixture in blocking IL-2-induced proliferation and, unexpectedly, was at least 65-fold more active than the mixture in blocking IL-15-induced proliferation. This dual inhibitory activity may be due to cross-linking of the IL-2R alpha and IL-2R beta, thus blocking IL-2 binding and possibly impeding the association of IL-2R beta with IL-15R. BF-IgG has potent immunosuppressant activities against both IL-2- and IL-15-mediated responses, and this antagonist could be more efficacious than HAT and/or HuMik beta 1 for the treatment of autoimmunity and the prevention of allograft rejection. Topics: Antibodies, Bispecific; Antibodies, Blocking; Antibody Affinity; Antibody Specificity; Binding Sites, Antibody; Cell Division; Clone Cells; Electrophoresis, Polyacrylamide Gel; Enzyme-Linked Immunosorbent Assay; Growth Inhibitors; Humans; Hybrid Cells; Interleukin-15; Leukemia, T-Cell; Receptors, Interleukin-2; Sodium Dodecyl Sulfate; Tumor Cells, Cultured | 1997 |
Characterisation of adriamycin- and amsacrine-resistant human leukaemic T cell lines.
Cell lines resistant to adriamycin and amsacrine were derived from cloned sublines of the human T cell line Jurkat. Most of the lines resemble atypical MDR cells (Danks et al., 1987; Beck et al., 1987). Thus, resistant Jurkat sublines were cross resistant to several topoisomerase II inhibiting drugs but had low or no resistance to other classes of drugs, resistance was not reversed by verapamil, Pgp was not overexpressed, and drug accumulation was unaltered in resistant compared to parental (control) sublines. Other findings were that anthracycline metabolism differed between resistant and parental sublines, and that resistant sublines displayed altered expression of small polypeptides (less than 20K MW) and an 85K MW protein. Drug resistant cells showed resistance to the production of drug induced cytogenetic aberrations, DNA breaks, and protein-DNA complexes. Resistance was not mediated by altered binding of drugs to DNA or by increased repair of DNA damage. Indirect evidence suggests that the resistant cells had an altered drug-DNA-topoisomerase II association. The study highlights the complex relationships between DNA breaks, cytogenetic aberrations, protein-DNA complexes and drug cytotoxicity, and shows that the relationships differ for adriamycin and amsacrine, suggesting some differences in the modes of action and/or resistance for the drugs and cell lines. Topics: Amsacrine; Clone Cells; Cytotoxicity, Immunologic; DNA Damage; DNA-Binding Proteins; DNA, Neoplasm; Doxorubicin; Drug Resistance; Electrophoresis, Polyacrylamide Gel; Fluorescence; Gene Amplification; Humans; Karyotyping; Leukemia, T-Cell; Neoplasm Proteins; Sodium Dodecyl Sulfate; Tumor Cells, Cultured | 1991 |