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催乳素和皮质醇对人自然杀伤细胞(NK)表面表达及自然细胞毒性受体(NKp46、NKp44和NKp30)功能的影响。

Effects of prolactin and cortisol on natural killer (NK) cell surface expression and function of human natural cytotoxicity receptors (NKp46, NKp44 and NKp30).

作者信息

Mavoungou E, Bouyou-Akotet M K, Kremsner P G

机构信息

Medical Research Unit, Albert Schweitzer Hospital, Lambaréné, Gabon.

出版信息

Clin Exp Immunol. 2005 Feb;139(2):287-96. doi: 10.1111/j.1365-2249.2004.02686.x.

Abstract

The surface density of the triggering receptors (e.g. NKp46 and NKp30) responsible for natural killer (NK) cell-mediated cytotoxicity determines the ability of NK cells to kill susceptible target cells. In this study, we show that prolactin up-regulates and cortisol down-regulates the surface expression of NKp46 and NKp30. The prolactin-mediated activation and the cortisol-mediated inhibition of natural cytotoxicity receptor (NCR) surface expression reflects gene regulation at the transcriptional level. NKp46 and NKp30 are the major receptors involved in the NK-mediated killing of K562, a human chronic myelogenous leukaemia cell line. Accordingly, the prolactin dramatically increased the NK-mediated killing of the K562 cell line, whereas cortisol abolished this activity. Our data suggest a mechanism by which prolactin activates the lytic function of NK cells, and cortisol inhibits the NK-mediated attack.

摘要

负责自然杀伤(NK)细胞介导的细胞毒性的触发受体(如NKp46和NKp30)的表面密度决定了NK细胞杀伤易感靶细胞的能力。在本研究中,我们发现催乳素上调而皮质醇下调NKp46和NKp30的表面表达。催乳素介导的自然细胞毒性受体(NCR)表面表达的激活和皮质醇介导的抑制反映了转录水平的基因调控。NKp46和NKp30是参与NK介导的对人慢性髓性白血病细胞系K562杀伤的主要受体。因此,催乳素显著增加了NK介导的对K562细胞系的杀伤,而皮质醇则消除了这种活性。我们的数据提示了一种机制,通过该机制催乳素激活NK细胞的裂解功能,而皮质醇抑制NK介导的攻击。

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