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生物化学损伤的成红细胞结合天然血清抗体并激活补体。

Biochemically damaged erythroblasts bind natural serum antibodies and activate complement.

作者信息

Wiener E, Dang R, Levy L, Wickramasinghe S N

机构信息

Department of Haematology, St Mary's Hospital Medical School, London, UK.

出版信息

Br J Exp Pathol. 1987 Dec;68(6):863-70.

Abstract

Friend leukaemia erythroblasts which had been damaged biochemically by treatment with inhibitors of cellular metabolism (sodium fluoride, sodium azide) or of protein synthesis (cycloheximide, puromycin) were incubated with heat-inactivated or fresh mouse serum and tested for surface-bound IgG and C3c, respectively, by reaction with FITC-immunoconjugates followed by flow-cytofluorometry. Erythroblasts exposed to sodium azide, cycloheximide or puromycin showed specific binding of IgG; the extent of binding was related to the concentration of the drugs and duration of treatment. Moreover, prolonged exposure of the cells to the inhibitors of protein synthesis lead to a dose-dependent activation of complement. The results suggest that the opsonization of biochemically-damaged Friend leukaemia erythroblasts with IgG and C3 may facilitate their interaction with macrophages.

摘要

用细胞代谢抑制剂(氟化钠、叠氮化钠)或蛋白质合成抑制剂(环己酰亚胺、嘌呤霉素)进行生化损伤的弗氏白血病成红细胞,与热灭活或新鲜小鼠血清一起孵育,然后分别通过与异硫氰酸荧光素免疫缀合物反应并进行流式细胞荧光测定法检测表面结合的IgG和C3c。暴露于叠氮化钠、环己酰亚胺或嘌呤霉素的成红细胞显示出IgG的特异性结合;结合程度与药物浓度和处理持续时间有关。此外,细胞长时间暴露于蛋白质合成抑制剂会导致补体的剂量依赖性激活。结果表明,用IgG和C3对生化损伤的弗氏白血病成红细胞进行调理可能会促进它们与巨噬细胞的相互作用。

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Impaired protein synthesis in erythroblasts enhances their phagocytosis by macrophages.
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