Nagler A, Lanier L L, Phillips J H
Becton-Dickinson Monoclonal Center, Inc., Mountain View, CA 94043.
J Immunol. 1988 Oct 1;141(7):2349-51.
NK cells are directly activated by rIL-2 and subsequently undergo rIL-2-dependent proliferation in vitro. Herein, we report that rIL-4 is a potent regulator of human NK cells. Although rIL-4 had no effect on the cytotoxic activity of resting NK cells, it was capable of inhibiting in a concentration-dependent manner the rIL-2-induced cytolytic activation of NK cells against NK cell-resistant tumor cell targets. rIL-4 acted directly on NK cells and did not require accessory cells. rIL-4-induced inhibition of NK cell activation was specific for rIL-2 in that activation of NK cell cytolysis by IFN-alpha was not affected. These results represent the first direct evidence that rIL-2 and IFN-alpha activate NK cells by different pathways. rIL-4 also effectively blocked the rIL-2-dependent proliferation of NK cells. The results presented in this study clearly demonstrate that rIL-4 is a potent regulator of IL-2-dependent mechanisms of NK cell activation and proliferation and thus may play an important physiologic role in vivo.
NK细胞可被重组白细胞介素-2(rIL-2)直接激活,随后在体外进行依赖rIL-2的增殖。在此,我们报告rIL-4是人类NK细胞的一种有效调节剂。尽管rIL-4对静息NK细胞的细胞毒性活性没有影响,但它能够以浓度依赖的方式抑制rIL-2诱导的NK细胞对NK细胞抗性肿瘤细胞靶标的溶细胞激活。rIL-4直接作用于NK细胞,不需要辅助细胞。rIL-4诱导的NK细胞激活抑制对rIL-2具有特异性,因为干扰素-α(IFN-α)对NK细胞溶解的激活不受影响。这些结果代表了rIL-2和IFN-α通过不同途径激活NK细胞的首个直接证据。rIL-4也有效阻断了NK细胞依赖rIL-2的增殖。本研究呈现的结果清楚地表明,rIL-4是NK细胞激活和增殖的IL-2依赖机制的一种有效调节剂,因此可能在体内发挥重要的生理作用。