Toda K, Miyachi Y, Kuribayashi K, Imamura S
J Clin Lab Immunol. 1986 Jul;20(3):129-31.
We have serially evaluated the basal and poly I: C-enhanced NK activity of BALB/c X C57BL/6 F1 nude mice (CB6F1-nu/nu) receiving repeated ultraviolet (UV) exposures with the interval of 2-5 weeks until overt skin tumor(s) developed. Chronic UV exposure induced a dose dependent suppression of basal splenic NK activity. The latent period between the initial UV treatment and the appearance of the first overt skin tumor was 19 weeks. After that time, incidence of tumor development gradually increased until it became 69% at the last inspection (27th week). 89% of the tumors inspected were fibrosarcoma and the remaining revealed squamous cell carcinoma. The UV-induced suppression of NK activity was restored by poly I:C treatment before the tumor appearance; however, this restorative effect was significantly reduced thereafter.
我们连续评估了接受重复紫外线（UV）照射的BALB/c×C57BL/6 F1裸鼠（CB6F1-nu/nu）的基础和聚肌苷酸:胞苷酸（poly I:C）增强的自然杀伤细胞（NK）活性，照射间隔为2至5周，直至出现明显的皮肤肿瘤。慢性紫外线照射诱导了基础脾脏NK活性的剂量依赖性抑制。从首次紫外线治疗到第一个明显皮肤肿瘤出现的潜伏期为19周。此后，肿瘤发生的发生率逐渐增加，直到最后一次检查（第27周）时达到69%。检查的肿瘤中有89%为纤维肉瘤，其余为鳞状细胞癌。紫外线诱导的NK活性抑制在肿瘤出现前通过聚肌苷酸:胞苷酸治疗得以恢复；然而，此后这种恢复作用显著降低。
