Chun M, Hoffmann M K
Lymphokine Res. 1982;1(4):91-8.
The mechanism by which interferon (IFN) and interleukin 2 (IL-2) activate NK cells has been examined. Added alone, either lymphokine activates NK cells; together they synergize. NK cells generated by IFN, IL-2 or IFN plus IL-2 are indistinguishable on the basis of their cell surface phenotype. Precursor NK cells are Qa5+, MK 2.2-, Ly-6- and effector NK cells are Qa5+, MK 2.2+, Ly-6+. Sequential factor addition showed that IFN must be present at the start of culture, whereas IL-2 could be added later with no loss of effect. Antibody to IFN was shown to block not only the action of IFN but also to prevent NK cell activation by IL-2. These results are taken to suggest that IFN initiates NK cell activation and IL-2 controls later stages. The synergistic effect of IL-2 is counteracted by cAMP. Considering the variety of systems in which IL-2 is active and the diversity of its effects, it is proposed that its antagonism with cAMP may be a basis for the biologic activity of IL-2.
人们已经研究了干扰素（IFN）和白细胞介素2（IL-2）激活自然杀伤细胞（NK细胞）的机制。单独添加时，这两种淋巴因子均可激活NK细胞；二者共同作用时则产生协同效应。由IFN、IL-2或IFN加IL-2产生的NK细胞，根据其细胞表面表型无法区分。前体NK细胞为Qa5 +、MK 2.2 -、Ly-6 -，效应NK细胞为Qa5 +、MK 2.2 +、Ly-6 +。顺序添加因子显示，IFN必须在培养开始时存在，而IL-2可以稍后添加且不影响效果。抗IFN抗体不仅能阻断IFN的作用，还能阻止IL-2激活NK细胞。这些结果表明，IFN启动NK细胞激活，而IL-2控制后期阶段。IL-2的协同效应被环磷酸腺苷（cAMP）抵消。考虑到IL-2发挥作用的多种系统及其效应的多样性，有人提出其与cAMP的拮抗作用可能是IL-2生物学活性的基础。
