阿拉伯糖胞嘧啶诱导多发性硬化症患者自然杀伤和抗体依赖性细胞毒性功能的改变。

D J Moody, J L Fahey, D Durkos-Smith, G W Ellison, L W Myers
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引用次数: 0

摘要

5例多发性硬化症患者每周接受阿糖胞嘧啶(araC)递增剂量治疗。起始剂量为50mg /M2,然后每周增加一次50mg /M2(除非毒性导致延迟)。剂量的决定是基于抗体依赖性细胞毒性(ADCC)或自然杀伤(NK)细胞毒性水平是否降低到低于对照范围2个标准差以上的水平。由于毒性,5名受试者中有2名剂量为500 mg/M2的阿糖胞嘧啶治疗停止。其余3例患者外周血中FcR+细胞百分比持续下降。从基线值减少的最大百分比从50%到76%不等。在相同剂量下,NK活性随之降低65%至83%。然而,在所有3例患者中,ADCC活性相对抵抗抑制。ADCC活动的最低点仅比基线最低值低16%至44%。与ADCC活性相比,AraC可降低FcR+细胞比例和NK细胞毒活性。
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Cytosine arabinoside induced changes in natural killer and antibody dependent cellular cytotoxicity functions in multiple sclerosis patients.

Five multiple sclerosis patients were treated weekly with cytosine arabinoside (araC) on an escalating dose schedule. The dose was initiated at 50 mg/M2 and then increased once each week by 50 mg/M2 (unless toxicity caused delay). Dosage decisions were based on whether or not the antibody-dependent cellular-cytotoxicity (ADCC) or natural killer (NK) cytotoxicity levels had been reduced to a level more than 2 standard deviations below the control range. Cytosine arabinoside treatment was discontinued in 2 of 5 subjects at doses of 500 mg/M2 due to toxicity. The 3 remaining patients demonstrated sustained reductions in the percentage of FcR+ cells in their peripheral blood. The maximum percentage reductions from the baseline values ranged from 50% to 76%. Concomitant reductions in the NK activity at the same doses ranged from 65% to 83%. ADCC activity in all 3 patients, however, was relatively resistant to suppression. The nadirs for the ADCC activity were only 16% to 44% below the baseline minimum. AraC was shown to reduce the proportion of FcR+ cells and NK cytotoxic activity in preference to ADCC activity.

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