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白细胞阳离子蛋白、髓鞘碱性蛋白和富含赖氨酸的组蛋白对C56启动的溶解作用的增强。

Potentiation of C56-initiated lysis by leucocyte cationic proteins, myelin basic proteins and lysine-rich histones.

作者信息

Baker P J, Lint T F, Siegel J, Kies M W, Gewurz H

出版信息

Immunology. 1976 Apr;30(4):467-73.

Abstract

Synthetic polycations such as poly-L-lysine (PLL) have recently been shown to enhance C56-initiated lysis by neutralization of serum-derived inhibitors of the C567 complex, collectively designated C567-INH. In the present report we have examined the effect of several naturally occurring polycations on C56-initiated lysis. Lysosomal granule extracts from rabbit peritoneal exudate cells were found to potentiate C56-initiated lysis via counteraction of C567-INH in the fluid phase; this was dependent upon the amount of C567-INH present and independent of cell concentration. The basic proteins of guinea-pig, bovine, and monkey myelin as well as lysine-rich histones also potentiated EC567 formation, but this effect seemed to occur predominantly at the cell surface. The presence of biologically derived cationic proteins at sites of complement activation during inflammation thus might lead to enhanced tissue damage by favouring the formation of cell-C567 intermediates by either or both of these mechanisms.

摘要

最近研究表明,诸如聚-L-赖氨酸(PLL)之类的合成聚阳离子可通过中和血清来源的C567复合物抑制剂(统称为C567-INH)来增强C56引发的细胞溶解作用。在本报告中,我们研究了几种天然存在的聚阳离子对C56引发的细胞溶解作用的影响。发现兔腹膜渗出细胞的溶酶体颗粒提取物可通过抵消液相中的C567-INH来增强C56引发的细胞溶解作用;这取决于C567-INH的含量,且与细胞浓度无关。豚鼠、牛和猴髓磷脂的碱性蛋白以及富含赖氨酸的组蛋白也增强了EC567的形成,但这种作用似乎主要发生在细胞表面。因此,在炎症过程中补体激活部位存在生物衍生的阳离子蛋白,可能通过上述一种或两种机制促进细胞-C567中间体的形成,从而导致组织损伤加剧。

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