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单核细胞诱导的 NK 细胞失活:活性氧和氮代谢物的作用。

Monocyte-induced NK cell inactivation: role of reactive oxygen and nitrogen metabolites.

机构信息

Department of Hematology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.

出版信息

Immunopharmacol Immunotoxicol. 2011 Mar;33(1):150-6. doi: 10.3109/08923973.2010.489051. Epub 2010 Jun 1.

Abstract

Here in a co-cultivation system of natural killer (NK) cells and K562 cells, monocytes (MO) and/or interleukin (IL)-2/phytohemagglutinin (PHA) were administered. After MO were administered, reactive oxygen metabolites (ROM)/reactive nitrogen metabolites (RNM) productions increased, while tumor necrosis factor (TNF)-β/interferon (IFN)-γ levels and NK cell cytotoxicity (NCC) decreased, the changes of which after administering tiopronin (TIP) or glutamylcysteinylglycine (GSH) were opposite. In conclusions, the activated MO could inhibit the NK cell activity to kill K562 cell by secreting ROM and RNM. And TIP and GSH could scavenge both ROM and RNM to reverse the inhibitory effect of MO.

摘要

在此自然杀伤 (NK) 细胞和 K562 细胞的共培养体系中,给予单核细胞 (MO) 和/或白细胞介素 (IL)-2/植物血凝素 (PHA)。给予 MO 后,活性氧代谢物 (ROM)/活性氮代谢物 (RNM) 的产生增加,而肿瘤坏死因子 (TNF)-β/干扰素 (IFN)-γ水平和 NK 细胞细胞毒性 (NCC) 降低,给予硫普罗宁 (TIP) 或谷氨酰半胱氨酸 (GSH) 后变化相反。总之,激活的 MO 可通过分泌 ROM 和 RNM 抑制 NK 细胞活性以杀伤 K562 细胞。TIP 和 GSH 可以清除 ROM 和 RNM,从而逆转 MO 的抑制作用。

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