白细胞介素-2局部分泌引发的小鼠肾细胞癌排斥反应。
Rejection of mouse renal cell carcinoma elicited by local secretion of interleukin-2.
作者信息
Hara I, Hotta H, Sato N, Eto H, Arakawa S, Kamidono S
机构信息
Department of Urology, Kobe University School of Medicine.
出版信息
Jpn J Cancer Res. 1996 Jul;87(7):724-9. doi: 10.1111/j.1349-7006.1996.tb00284.x.
We introduced the interleukin-2 (IL-2) gene into mouse renal cell carcinoma (RenCa) in order to examine the mechanism of tumor rejection. IL-2 gene-transfected RenCa (RenCa/IL-2Hi) exhibited marked retardation of tumor growth when implanted in a syngeneic host. Growth retardation of RenCa/IL-2Hi was also observed in athymic nude mice even after depletion of natural killer (NK) cells by treatment with anti-asialo GM1 antibody. Histological analysis of RenCa/IL-2Hi tumors disclosed non-specific inflammatory changes in syngeneic hosts. Co-injection of Bacillus Calmette Guerin with RenCa/IL-2Hi considerably enhanced the anti-tumor effects. Taken together, these findings strongly suggest that in situ IL-2 production leads to tumor rejection through non-specific inflammatory responses without participation of T cells and NK cells. On the other hand, the syngeneic mice that had rejected RenCa/IL-2Hi acquired immunity against parental RenCa, suggesting possible participation of memory T cells in the second rejection of the tumor.
为了研究肿瘤排斥反应的机制，我们将白细胞介素-2（IL-2）基因导入小鼠肾细胞癌（RenCa）中。将IL-2基因转染的RenCa（RenCa/IL-2Hi）接种于同基因宿主时，肿瘤生长明显迟缓。在用抗唾液酸GM1抗体处理耗尽自然杀伤（NK）细胞后，在无胸腺裸鼠中也观察到RenCa/IL-2Hi的生长迟缓。对RenCa/IL-2Hi肿瘤的组织学分析显示同基因宿主中存在非特异性炎症变化。将卡介苗与RenCa/IL-2Hi共同注射可显著增强抗肿瘤作用。综上所述，这些发现强烈表明原位产生IL-2可通过非特异性炎症反应导致肿瘤排斥，而无需T细胞和NK细胞参与。另一方面，排斥RenCa/IL-2Hi的同基因小鼠获得了针对亲本RenCa的免疫力，这表明记忆T细胞可能参与了肿瘤的二次排斥反应。
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