Lymphokine maintains macrophage activation for tumor cell killing by interfering with the negative regulatory effect of prostaglandin E2.
Lymphokine maintains macrophage activation for tumor cell killing by interfering with the negative regulatory effect of prostaglandin E2.
复制标题
淋巴因子通过干扰前列腺素 E2 的负调节作用来维持巨噬细胞的活化，从而杀死肿瘤细胞。
作者：
S. Taffet;J. Pace;S. Russell
用细菌脂多糖（LPS）激活的小鼠驻留腹腔巨噬细胞在体外迅速丧失其杀死肿瘤细胞的能力。这种杀伤力的丧失此前被归因于脂多糖刺激的巨噬细胞产生的前列腺素E（PGE）的作用。在本研究中暴露于LPS和部分纯化的淋巴因子的巨噬细胞没有失去细胞溶解活性，尽管这些细胞产生的PGE量与对照组相比没有减少。在这些条件下，由于淋巴因子降低了活化的巨噬细胞对PGE负调节作用的敏感性，因此细胞溶解活性被保留。淋巴因子效应的机制尚不清楚;然而，巨噬细胞对激素反应性的普遍抑制似乎并不涉及，因为淋巴因子并没有降低巨噬细胞的环AMP反应，在整个细胞的基础上测量，在它们暴露于PGE后。
Mouse resident peritoneal macrophages activated with bacterial lipopolysaccharide (LPS) rapidly lost their ability to kill tumor cells in vitro. Such loss of killing has previously been attributed to the effects of prostaglandin E (PGE) produced by the LPS-stimulated macrophages. Macrophages exposed in the current study to both LPS and partially purified lymphokine did not lose cytolytic activity, in spite of the fact that these cells produced undiminished amounts of PGE, compared to controls. Cytolytic activity was shown to be retained under these conditions because lymphokine decreased the sensitivity of activated macrophages to the negative regulatory effects of PGE. The mechanism responsible for the lymphokine effect is not known; however, generalized inhibition of macrophage responsiveness to the hormone does not appear to be involved because lymphokine did not reduce the cyclic AMP response of macrophages, measured on a whole cell basis, after they were exposed to PGE.