Macrophage cytotoxicity: interleukin 1 as a mediator of tumor cytostasis.
Macrophage cytotoxicity: interleukin 1 as a mediator of tumor cytostasis.
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巨噬细胞的细胞毒性：白介素 1 作为肿瘤细胞抑制的介质。
DOI：
10.4049/jimmunol.136.1.340
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发表时间：
1986
影响因子：
4.4
通讯作者：
D. Gemsa
中科院分区：
文献类型：
--
作者：
D. Lovett;B. Kozan;M. Hadam;K. Resch;D. Gemsa
纯化的巨噬细胞白细胞介素1（IL 1）诱导两种常用的肿瘤靶细胞系，人髓系K562和小鼠T淋巴瘤Eb的增殖的浓度依赖性抑制。相反，肥大细胞瘤衍生的P815细胞不受抑制。IL 1的细胞抑制作用与直接细胞毒性无关，并且仅部分可逆。前列腺素E或干扰素似乎没有介导这些影响。IL-1处理的多能K562细胞没有发现诱导特异性分化的形态学证据。经IL 1处理的K562细胞的流式细胞仪分析显示转铁蛋白受体密度迅速下降，而HLA-A、B、C抗原密度延迟但高度显著地增加。这些发现为经常报道的巨噬细胞对肿瘤细胞的细胞生长抑制作用提供了一种解释，并且也表明IL 1，像干扰素一样，可以增强I类MHC抗原的表达。这些观察结果进一步扩展了IL 1作用的范围，并强调了这种单核因子在巨噬细胞抗肿瘤活性中的基本和直接作用。
Purified macrophage interleukin 1 (IL 1) induced a concentration-dependent inhibition of the proliferation of two commonly used tumor cell target lines, the human myeloid K562 and the murine T lymphoma Eb. In contrast, mastocytoma-derived P815 cells were not inhibited. The cytostatic action of IL 1 was not associated with direct cytotoxicity and was only partially reversible. PGE or interferon did not appear to mediate these effects. IL 1 treatment of the multipotential K562 cells revealed no morphologic evidence for the induction of specific differentiation. FACS analysis of IL 1-treated K562 cells showed a rapid decrease in transferrin receptor density, and a more delayed, but highly significant, increase in HLA-A,B,C antigen density. These findings provide one explanation for the frequently reported macrophage cytostatic actions against tumor cells, and indicate as well that IL 1, like interferon, may enhance the expression of Class I MHC antigens. These observations further extend the range of IL 1 actions and underscore the fundamental and direct role of this monokine in macrophage antitumor activity.