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C567引发的淋巴细胞溶解:现象描述及其受C567抑制剂调控的研究

C567-initiated cytolysis of lymphoid cells: description of the phenomenon and studies on its control by C567 inhibitors.

作者信息

Baker P J, Lint T F, Mortensen R F, Gewurz H

出版信息

J Immunol. 1977 Jan;118(1):198-202.

PMID:830747
Abstract

Cells of the Raji human lymphoblastoid line, when pretreated with the metabolic inhibitor puromycin were found to be susceptible to killing by the isolated proteins of the complement attack mechanism (C5-9). Incubation of 51Cr-labeled lymphoblastoid cells with purified C56 and C7 resulted in the formation of a lymphoblast-C567 (LC567) intermediate, and the addition of purified human C8 and C9 resulted in release of 51Cr from these cells. Serum C567 inhibitors (C567-INH), purified human lipoproteins, and dextran sulfate, each previously shown to inhibit the attachment of the C567 trimolecular complex to erythrocytes, also inhibited the formation of LC567, and as a consequence, C56-initiated cytotoxicity; the polycation protamine sulfate counteracted the inhibitory effect of dextran sulfate. Thus, the potential for damage of bystander nucleated cells exists when C56 is generated in solution, and is influenced by agents known to modulate the hemolytic activity of C567. It is suggested that these mechanisms may be involved in the control of the function as well as the viability of various nucleated cells.

摘要

当用代谢抑制剂嘌呤霉素预处理时,发现拉吉人淋巴母细胞系的细胞对补体攻击机制(C5 - 9)的分离蛋白杀伤敏感。用纯化的C56和C7孵育51Cr标记的淋巴母细胞会导致形成淋巴母细胞 - C567(LC567)中间体,添加纯化的人C8和C9会导致这些细胞释放51Cr。血清C567抑制剂(C567 - INH)、纯化的人脂蛋白和硫酸葡聚糖,之前均显示可抑制C567三分子复合物与红细胞的结合,它们也抑制LC567的形成,因此,抑制了C56引发的细胞毒性;聚阳离子硫酸鱼精蛋白抵消了硫酸葡聚糖的抑制作用。因此,当溶液中产生C56时,旁观者有核细胞存在受损的可能性,并且受到已知可调节C567溶血活性的物质的影响。提示这些机制可能参与各种有核细胞功能以及活力的控制。

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