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由于靶细胞膜通过替代途径激活C3而导致的补体依赖性细胞毒性。

Complement-dependent cellular cytotoxicity due to alternative pathway C3 activation by the target cell membrane.

作者信息

Yefenof E, Yron I, Klein E

出版信息

Cell Immunol. 1984 Sep;87(2):698-702. doi: 10.1016/0008-8749(84)90038-8.

DOI:10.1016/0008-8749(84)90038-8
PMID:6467388
Abstract

The cytotoxic activity of human blood lymphocytes toward Raji cells was strongly elevated when human serum (HS) was included in the cytotoxicity assay. This phenomenon also occurred when the effector cells were activated by interferon (IFN). Hypogammaglobulinemic serum (HyS) and heat-inactivated serum could also augment cytotoxicity, but C3-depleted serum was inefficient. IFN treatment of Raji cells decreased their sensitivity to lysis and this effect was counteracted by addition of HS to the system. It is likely that C3 activation by, and deposition on, Raji cells when used as targets for cytotoxicity facilitate their recognition and lysis by lymphocytes. These events may represent one mechanism operating in the natural killing phenomenon.

摘要

当细胞毒性试验中加入人血清(HS)时,人血淋巴细胞对Raji细胞的细胞毒性活性显著升高。当效应细胞被干扰素(IFN)激活时,也会出现这种现象。低丙种球蛋白血症血清(HyS)和热灭活血清也可增强细胞毒性,但C3缺陷血清则无效。用IFN处理Raji细胞会降低其对裂解的敏感性,而向系统中加入HS可抵消这种作用。当Raji细胞作为细胞毒性的靶细胞时,其C3的激活和沉积可能有助于淋巴细胞对它们的识别和裂解。这些事件可能代表了自然杀伤现象中的一种作用机制。

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引用本文的文献

1
Complement-dependent cellular cytotoxicity: lymphoblastoid lines that activate complement component 3 (C3) and express C3 receptors have increased sensitivity to lymphocyte-mediated lysis in the presence of fresh human serum.补体依赖的细胞毒性:激活补体成分3(C3)并表达C3受体的淋巴母细胞系在新鲜人血清存在的情况下,对淋巴细胞介导的裂解敏感性增加。
Proc Natl Acad Sci U S A. 1985 Aug;82(16):5470-4. doi: 10.1073/pnas.82.16.5470.
2
Biology of natural killer cells.自然杀伤细胞生物学
Adv Immunol. 1989;47:187-376. doi: 10.1016/s0065-2776(08)60664-1.