作者: MR Jadus , MC Irwin , MR Irwin , RD Horansky , S Sekhon
DOI: 10.1182/BLOOD.V87.12.5232.BLOODJOURNAL87125232
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摘要: NBXFO hybridoma cells produced both the membrane and secreted isoforms of macrophage colony-stimulating factor (M-CSF). Murine bone marrow stimulated by form M-CSF (sM-CSF) became Mac1+, Mac2+, Mac3+, F4/80+ macrophages that inhibited growth cells, but not L1210 or P815 tumor cells. In cytotoxicity studies, M- CSF activated freshly isolated killed in presence polymyxin B, eliminating possibility contaminating lipopolysaccharide (LPS) was responsible for delivery cytotoxic signal. Retroviral-mediated transfection T9 glioma with gene isoform (mM-CSF), M-CSF, transferred ability to kill these transfected a mM-CSF dose- dependent manner. Macrophage-mediated killing clone blocked using 100-fold excess recombinant M-CSF. Catalase, superoxide dismutase, nitric oxide inhibitor, N-omega- nitro-arginine methyl ester (NAME), did effect against transfectant clones. parental when cultured an equal number were killed, indicating specific target cell macrophages. Electron microscopy showed capable phagocytosizing bearing cells; this suggested possible mechanism cytotoxicity. This study indicates provides necessary binding triggering molecules through which can initiate direct