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Increased sensitivity of cholera toxin B treated K562 cells to natural killer cells.

机译:霍乱毒素B处理的K562细胞对自然杀伤细胞的敏感性增加。

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Cholera toxin B-subunit (CTB) treatment of K562 erythroleukemia cells increased their sensitivity to be killed by NK-92 cells with more than 10%, compared to untreated cells. A similar treatment of non-T, non-B acute lymphoblastic REH leukemia cells, known to be unsensitive to NK cell mediated cytotoxicity, did not have any impact at all. Visualization of the cross-linked ganglioside(M1) (GM(1)) using fluorescent labeled CTB, indicated accumulation of the fluorescence to one cap and a few smaller patches in both type of cells. Additional cross-linking using anti-CTB antibodies further accentuated capping and increased lysis in the case of K562 cells. Blocking experiments performed with anti-MICA/B, ULBP-2 and/or CD59 antibodies could not inhibit the increased sensitivity mediated by CTB.
机译:与未经处理的细胞相比,霍乱毒素B亚基(CTB)处理K562红白血病细胞的敏感性被NK-92细胞杀死的敏感性提高了10%以上。已知对NK细胞介导的细胞毒性不敏感的非T,非B急性淋巴细胞REH白血病细胞的类似治疗根本没有任何影响。使用荧光标记的CTB可视化交联的神经节苷脂(M1)(GM(1)),表明荧光在两种类型的细胞中积累到一个帽和一些较小的斑块。在使用K562细胞的情况下,使用抗CTB抗体进行的其他交联进一步加重了封端并增加了裂解。用抗MICA / B,ULBP-2和/或CD59抗体进行的阻断实验不能抑制CTB介导的敏感性增加。

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