Smyth M J, Ortaldo J R
Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201.
J Immunol. 1991 Feb 15;146(4):1380-4.
The effects of IL-6 and IL-2 on highly purified, human peripheral blood large granular lymphocytes (LGL) were investigated and compared. IL-6 enhanced LGL NK activity in a dose-dependent manner against K562, however IL-2 was a more potent stimulus of LGL NK function. Neither IL-2 nor IL-6 increased LGL cytotoxic potential in a parallel estimation of heteroconjugated antibody (anti-CD16 x anti-nitrophenyl mAb)-dependent cytotoxicity against nitrophenyl-modified YAC. Unlike IL-2, IL-6 did not significantly induce LGL lymphokine-activated killer activity, LGL proliferation, or LGL lymphokine production. In particular, IL-6 did not stimulate detectable LGL IL-2 production or IL-2R modulation, and mAb to the p75 IL-2R had no effect on IL-6 induction of LGL NK activity. Therefore, in the absence of T cells, IL-6 provided an IL-2-independent signal to LGL that resulted in augmentation of their NK activity without stimulating their proliferation or other LGL functions.
研究并比较了白细胞介素-6（IL-6）和白细胞介素-2（IL-2）对高度纯化的人外周血大颗粒淋巴细胞（LGL）的作用。IL-6以剂量依赖方式增强LGL对K562的自然杀伤（NK）活性，然而IL-2对LGL的NK功能是更强效的刺激物。在对硝基苯基修饰的YAC进行异源结合抗体（抗-CD16×抗-硝基苯基单克隆抗体）依赖性细胞毒性的平行评估中，IL-2和IL-6均未增加LGL的细胞毒性潜能。与IL-2不同，IL-6不会显著诱导LGL淋巴因子激活的杀伤活性、LGL增殖或LGL淋巴因子产生。特别是，IL-6不会刺激可检测到的LGL白细胞介素-2产生或白细胞介素-2受体调节，并且针对p75白细胞介素-2受体的单克隆抗体对IL-6诱导LGL的NK活性没有影响。因此，在没有T细胞的情况下，IL-6向LGL提供了一个不依赖IL-2的信号，导致其NK活性增强，而不会刺激其增殖或其他LGL功能。
