前列腺素E2对人自然杀伤细胞和淋巴因子激活的杀伤细胞细胞毒性及分化的抑制作用。

Inhibition of human NK cell and LAK cell cytotoxicity and differentiation by PGE2.

作者信息

Leung K H

机构信息

E. I. du Pont de Nemours and Co., Medical Products Department, Glenolden, Pennsylvania 19036.

出版信息

Cell Immunol. 1989 Oct 15;123(2):384-95. doi: 10.1016/0008-8749(89)90298-0.

DOI:10.1016/0008-8749(89)90298-0

PMID:2507171

Abstract

Activation of natural killer (NK) activity K562 target cells from nonadherent (NA) lymphocytes by interleukin 2 (IL-2) was inhibited marginally PGE2 (30-3000 nM). PGE2 did not effectively suppress the NK activity of IL-2-activated cells. The NK activation and acquisition of resistance to PGE2-mediated suppression of NK activity were dependent on protein synthesis. When NA cells were incubated with IL-2 for 3 or more days to generate lymphokine-activated killer (LAK) activity against Raji target cells, PGE2 only partially inhibited the activation of NK/LAK activity by an optimal dose of IL-2 (10 U/ml). The activation of NK/LAK activity by a suboptimal dose of IL-2 (0.1 U/ml) was inhibited by PGE2. When the NK/LAK activity of IL-2-activated cells was assessed in the presence or absence of PGE2, the LAK activity was more sensitive than the NK activity to PGE2-mediated suppression.

摘要

白细胞介素2（IL-2）激活非黏附（NA）淋巴细胞的天然杀伤（NK）活性以杀伤K562靶细胞时，前列腺素E2（PGE2，30 - 3000 nM）仅有轻微抑制作用。PGE2不能有效抑制IL-2激活细胞的NK活性。NK激活以及获得对PGE2介导的NK活性抑制的抗性均依赖于蛋白质合成。当NA细胞与IL-2孵育3天或更长时间以产生针对Raji靶细胞的淋巴因子激活的杀伤细胞（LAK）活性时，PGE2仅部分抑制最佳剂量IL-2（10 U/ml）对NK/LAK活性的激活。PGE2抑制次优剂量IL-2（0.1 U/ml）对NK/LAK活性的激活。当在有或无PGE2的情况下评估IL-2激活细胞的NK/LAK活性时，LAK活性比NK活性对PGE2介导的抑制更敏感。