Toshitani A, Taniguchi K, Kawano Y, Nomoto K
Cell Immunol. 1987 Aug;108(1):188-202. doi: 10.1016/0008-8749(87)90203-6.
We investigated the manner in which rIL-2 induced effectors in vitro (LAK cells), which, like NK cells, lyse targets nonspecifically and discriminate nonself, and how H-2 as the self-marker affects the LAK cell killing mechanism. NK cells showed an appreciably higher killing activity to B16 melanoma H-2- cells than to H-2+ cells. In contrast, LAK cells lysed more efficiently to H-2+ cells. The in vivo experiments showed that the NK cells prevented pulmonary metastasis of B16 H-2- cells in the normal syngeneic host, whereas the transferred LAK cells had a preferential inhibitory effect on the pulmonary metastasis of B16 H-2+ cells in the immunodeficient syngeneic hosts. Taken together, these results show that the H-2-encoded or H-2-associated molecules contribute to the triggering signal in the lysis by LAK cells, whereas the NK cells recognize the reduced self H-2 expression on the targets, thereby contributing to a trigger of the lysis.
我们研究了重组白细胞介素-2(rIL-2)在体外诱导效应细胞(淋巴因子激活的杀伤细胞,即LAK细胞)的方式,该细胞与自然杀伤细胞(NK细胞)一样,能非特异性地裂解靶细胞并识别非己成分,同时还研究了作为自身标记的H-2如何影响LAK细胞的杀伤机制。NK细胞对B16黑色素瘤H-2-细胞的杀伤活性明显高于对H-2+细胞的杀伤活性。相反,LAK细胞对H-2+细胞的裂解效率更高。体内实验表明,在正常同基因宿主中,NK细胞可阻止B16 H-2-细胞的肺转移,而在免疫缺陷的同基因宿主中,转移的LAK细胞对B16 H-2+细胞的肺转移具有优先抑制作用。综上所述,这些结果表明,H-2编码的或与H-2相关的分子在LAK细胞介导的裂解中起触发信号的作用,而NK细胞识别靶细胞上自身H-2表达的降低,从而促成裂解的触发。