Pace J L, Russell S W, Torres B A, Johnson H M, Gray P W
J Immunol. 1983 May;130(5):2011-3.
Mouse macrophages become activated to kill tumor cells by traversing a series of steps (1-3). The first of these does not cause the expression of cytolytic activity; instead, it primes macrophages to respond to a second signal(s) that then triggers the onset of killing (4-7). The mediator that is responsible for priming is contained, along with other lymphokines, in the culture supernatants of concanavalin A-stimulated spleen cells (5-7) cloned T lymphocytes (8), or some T cell hybridomas (9). Close association has been noted between macrophage priming activity and antiviral activity that is attributable to gamma interferon (10-12). However, unequivocal evidence that the two activities are products of the same molecule has not been available. We now how conclusively by using mouse gamma interferon (MulFN-gamma)3 produced by recombinant DNA technology that, in addition to antiviral activity, this lymphokine has the capacity to induce the priming step in the process of macrophage activation for tumor cell killing.
小鼠巨噬细胞通过一系列步骤（1 - 3）被激活以杀死肿瘤细胞。其中第一步不会导致细胞溶解活性的表达；相反，它使巨噬细胞对第二个信号作出反应，然后触发杀伤作用的开始（4 - 7）。负责引发的介质与其他淋巴因子一起，存在于伴刀豆球蛋白A刺激的脾细胞（5 - 7）、克隆的T淋巴细胞（8）或一些T细胞杂交瘤（9）的培养上清液中。已经注意到巨噬细胞引发活性与可归因于γ干扰素的抗病毒活性之间存在密切关联（10 - 12）。然而，尚无确凿证据表明这两种活性是同一分子的产物。我们现在通过使用重组DNA技术产生的小鼠γ干扰素（MulFN - γ）3确凿地证明，除了抗病毒活性外，这种淋巴因子还具有在巨噬细胞激活以杀伤肿瘤细胞的过程中诱导引发步骤的能力。
