白细胞介素4（IL-4）通过抑制白细胞介素2受体α、β和γ的表达，阻断IL-2诱导的蜕膜CD16-CD56bright自然杀伤细胞的自然杀伤活性增加和DNA合成。

Interleukin 4 (IL-4) blocks the IL-2-induced increased in natural killer activity and DNA synthesis of decidual CD16-CD56bright NK cells by inhibiting expression of the IL-2 receptor alpha, beta, and gamma.

作者信息

Saito S, Umekage H, Nishikawa K, Morii T, Narita N, Enomoto M, Sakakura S, Harada N, Ichijo M, Morikawa H

机构信息

Department of Obstetrics and Gynecology, Nara Medical University, Japan.

出版信息

Cell Immunol. 1996 May 25;170(1):71-7. doi: 10.1006/cimm.1996.0135.

DOI:10.1006/cimm.1996.0135

PMID:8660801

Abstract

The natural killer (NK) activity and DNA synthesis of decidual CD16-CD56bright NK cells were markedly elevated by treatment with interleukin 2 (IL-2). IL-4 did not affect NK activity or DNA synthesis of decidual CD16-CD56bright NK cells, but inhibited the IL-2-induced NK activity and DNA synthesis in a dose-dependent manner. Flow cytometry of decidual mononuclear cells cultured in IL-2 or IL-4 or both IL-2 and IL-4 demonstrated IL-4 inhibition of the expression of the IL-2 receptor alpha (IL-2R alpha), IL-2R beta, and IL-2R gamma on decidual CD16-CD56bright NK cells. This suggests that IL-4 blocks the IL-2-induced NK activity and DNA synthesis of decidual CD16-CD56bright NK cells by inhibiting the expression of IL-2R alpha, IL-2R beta, and IL-2R gamma.

摘要

用白细胞介素2（IL-2）处理后，蜕膜CD16-CD56bright自然杀伤（NK）细胞的NK活性和DNA合成显著升高。IL-4不影响蜕膜CD16-CD56bright NK细胞的NK活性或DNA合成，但以剂量依赖的方式抑制IL-2诱导的NK活性和DNA合成。对在IL-2或IL-4或IL-2和IL-4两者中培养的蜕膜单个核细胞进行流式细胞术分析，结果显示IL-4抑制蜕膜CD16-CD56bright NK细胞上IL-2受体α（IL-2Rα）、IL-2Rβ和IL-2Rγ的表达。这表明IL-4通过抑制IL-2Rα、IL-2Rβ和IL-2Rγ的表达来阻断IL-2诱导的蜕膜CD16-CD56bright NK细胞的NK活性和DNA合成。