Bachwich P R, Chensue S W, Larrick J W, Kunkel S L
Biochem Biophys Res Commun. 1986 Apr 14;136(1):94-101. doi: 10.1016/0006-291x(86)90881-8.
We have investigated the effect of tumor necrosis factor on the release of interleukin-1 and PGE2 from murine resident peritoneal macrophages. Tumor necrosis factor causes an increase in the production of interleukin-1 and PGE2 with a maximum induction for both noted at 5.9 X 10(-8) M. While indomethacin decreased tumor necrosis factor induced PGE2 production, this cyclooxygenase inhibitor augmented tumor necrosis factor induced interleukin-1 production. Our data suggests that tumor necrosis factor may be an important immunopotentiating agent in addition to its previously described cytolytic and metabolic activities.
我们研究了肿瘤坏死因子对小鼠腹腔常驻巨噬细胞释放白细胞介素-1和前列腺素E2的影响。肿瘤坏死因子可导致白细胞介素-1和前列腺素E2的产生增加，两者的最大诱导浓度均为5.9×10⁻⁸M。虽然吲哚美辛可降低肿瘤坏死因子诱导的前列腺素E2产生，但这种环氧化酶抑制剂却增强了肿瘤坏死因子诱导的白细胞介素-1产生。我们的数据表明，肿瘤坏死因子除了具有先前描述的细胞溶解和代谢活性外，可能还是一种重要的免疫增强剂。
