Young M R, Hoover C S
J Natl Cancer Inst. 1986 Aug;77(2):425-9.
The capacity to generate cytotoxic cells toward Lewis lung carcinoma (LLC) in mixed cultures of stimulator LLC and responder spleen cells of LLC-bearing C57BL/6 mice was monitored during the course of tumor growth. The cytotoxic response of mice bearing tumors that were not yet palpable was enhanced. However, as palpable tumors developed and tumor growth progressed, their cytotoxic capacity became suppressed. Concurrent with this decline in cytotoxic capacity, there was an increase in systemic immunoreactive prostaglandin E2 (PGE2) concentrations in tumor-bearing mice. Administration of indomethacin, a prostaglandin synthesis inhibitor, to LLC-bearing mice prevented the rise in PGE2 concentrations and the suppression in cytotoxic capacity toward LLC. A relationship between the elevated immunoreactive PGE2 levels, suppression in cytotoxic capacity, and progressive tumor growth was indicated when administration of indomethacin to tumor-bearing mice also reduced the rate of tumor development.
在荷Lewis肺癌(LLC)的C57BL/6小鼠肿瘤生长过程中,监测了刺激物LLC与荷瘤小鼠反应性脾细胞混合培养物中产生针对LLC的细胞毒性细胞的能力。尚未触及肿瘤的小鼠的细胞毒性反应增强。然而,随着可触及肿瘤的出现和肿瘤生长的进展,它们的细胞毒性能力受到抑制。伴随着细胞毒性能力的这种下降,荷瘤小鼠全身免疫反应性前列腺素E2(PGE2)浓度增加。给荷LLC小鼠施用前列腺素合成抑制剂吲哚美辛,可防止PGE2浓度升高以及对LLC细胞毒性能力的抑制。当给荷瘤小鼠施用吲哚美辛也降低了肿瘤发展速度时,提示免疫反应性PGE2水平升高、细胞毒性能力抑制与肿瘤进行性生长之间存在关联。