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肿瘤介导的免疫抑制:通过前列腺素合成抑制剂进行预防。

Tumor-mediated immunosuppression: prevention by inhibitors of prostaglandin synthesis.

作者信息

Grinwich K D, Plescia O J

出版信息

Prostaglandins. 1977;14(6):1175-82. doi: 10.1016/0090-6980(77)90294-5.

Abstract

The addition of MC16 tumor cells (a prostaglandin E2-producing cell line induced in C57BL/6J mice by methylcholanthrene) to cultures of cells to sheep red blood cells. This inhibition can be blocked by adding to the cultures prostaglandin synthetase inhibitors, such as indomethacin, flufenamic acid and aspirin. These MC16 tumor cells are also immunosuppressive in vivo. Mice bearing the syngeneic MC16 tumor become unresponsive to sheep red blood cells as the tumor grows. As in the in vitro test system, inhibitors of prostaglandin synthetases seem to block the immunosuppressive activity of MC16 cells in vivo since tumor-bearing mice, treated therapeutically with indomethacin, responded normally in their production of antibody to sheep red blood cells.

摘要

将MC16肿瘤细胞(一种由甲基胆蒽在C57BL/6J小鼠中诱导产生的能产生前列腺素E2的细胞系)添加到细胞与绵羊红细胞的培养物中。这种抑制作用可通过向培养物中添加前列腺素合成酶抑制剂(如消炎痛、氟灭酸和阿司匹林)来阻断。这些MC16肿瘤细胞在体内也具有免疫抑制作用。携带同基因MC16肿瘤的小鼠随着肿瘤生长对绵羊红细胞变得无反应。与体外测试系统一样,前列腺素合成酶抑制剂似乎能阻断MC16细胞在体内的免疫抑制活性,因为用消炎痛进行治疗的荷瘤小鼠在产生针对绵羊红细胞的抗体方面反应正常。

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