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木瓜蛋白酶处理的淋巴细胞增强补体依赖性细胞毒性的机制:经典途径C3转化酶稳定性增加的证据。

Mechanism of enhanced complement-dependent cytotoxicity of papain-treated lymphocytes: evidence for increased stability of classical pathway C3 convertase.

作者信息

Lublin D M, Grumet F C

出版信息

J Immunol. 1982 Feb;128(2):866-70.

PMID:6915075
Abstract

The mechanisms of enhanced antibody-mediated, complement-dependent cytotoxicity caused by proteolytic treatment of cells was studied in a model system based on HLA microlymphocytotoxicity methods. In this model, papain treatment of lymphocytes resulted in a) no change in antibody binding, b) a slight decrease in initial binding of C4, c) a marked increase in stability of cell-bound C4b, resulting in d) an increase of cell-bound C3, and e) no increase in lytic efficiency of the C5b-9 membrane attack complex. We conclude that the most important step in papain enhancement of lysis of lymphocytes is an increased stability of cell-bound C4b, possibly through decreased surface binding of C4-bp. This mechanism may be relevant to the pathologically increased lysis of cells occurring in patients with hereditary erythroblastic multinuclearity with a positive acidified-serum test (HEM-PAS).

摘要

在基于HLA微量淋巴细胞毒性方法的模型系统中,研究了细胞经蛋白水解处理后抗体介导的、补体依赖性细胞毒性增强的机制。在该模型中,用木瓜蛋白酶处理淋巴细胞导致:a)抗体结合无变化;b)C4初始结合略有下降;c)细胞结合的C4b稳定性显著增加,导致d)细胞结合的C3增加;e)C5b-9膜攻击复合物的裂解效率无增加。我们得出结论,木瓜蛋白酶增强淋巴细胞裂解的最重要步骤是细胞结合的C4b稳定性增加,可能是通过减少C4-bp的表面结合实现的。这种机制可能与遗传性红细胞多核症伴酸化血清试验阳性(HEM-PAS)患者中细胞病理性裂解增加有关。

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Mechanism of enhanced complement-dependent cytotoxicity of papain-treated lymphocytes: evidence for increased stability of classical pathway C3 convertase.木瓜蛋白酶处理的淋巴细胞增强补体依赖性细胞毒性的机制:经典途径C3转化酶稳定性增加的证据。
J Immunol. 1982 Feb;128(2):866-70.
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引用本文的文献

1
The alternative pathway of complement.补体替代途径
Springer Semin Immunopathol. 1984;7(2-3):163-92. doi: 10.1007/BF01893019.