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被多形核白细胞氧化的低密度脂蛋白会抑制自然杀伤细胞的活性。

Low-density lipoprotein oxidized by polymorphonuclear leukocytes inhibits natural killer cell activity.

作者信息

Tanabe F, Sato A, Ito M, Ishida E, Ogata M, Shigeta S

机构信息

Department of Bacteriology, Fukushima Medical College, Japan.

出版信息

J Leukoc Biol. 1988 Mar;43(3):204-10. doi: 10.1002/jlb.43.3.204.

Abstract

We studied the effect of low-density lipoprotein (LDL) oxidized by opsonized zymosan-stimulated polymorphonuclear leukocytes (PMN) on natural killer (NK) cell activity. Oxidized LDL inhibited NK cell activity in a dose-dependent manner, whereas normal LDL left it unaffected. However, oxidized LDL did not inhibit antibody-dependent cell-mediated cytotoxicity (ADCC). Moreover, a positive correlation was observed between the amount of thiobarbituric acid-reacting substances (TBARS) on the sample of oxidized LDL and the degree of inhibition of NK cell activity. We also showed that oxidized LDL suppressed the binding capacity of purified large granular lymphocytes (LGL) to target cells without changing the lytic activity. These results therefore suggest that activated PMN can modulate NK cell activity by oxidizing LDL.

摘要

我们研究了经调理酵母聚糖刺激的多形核白细胞(PMN)氧化的低密度脂蛋白(LDL)对自然杀伤(NK)细胞活性的影响。氧化型LDL以剂量依赖的方式抑制NK细胞活性,而正常LDL则无此影响。然而,氧化型LDL并不抑制抗体依赖的细胞介导的细胞毒性(ADCC)。此外,在氧化型LDL样品上硫代巴比妥酸反应物质(TBARS)的量与NK细胞活性的抑制程度之间观察到正相关。我们还表明,氧化型LDL在不改变裂解活性的情况下抑制纯化的大颗粒淋巴细胞(LGL)与靶细胞的结合能力。因此,这些结果表明活化的PMN可通过氧化LDL来调节NK细胞活性。

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