De Mik H J, Koten J W, Maas R A, Dullens H F, Den Otter W
Instituut voor Pathologie, Academisch Ziekenhuis Utrecht, The Netherlands.
In Vivo. 1991 Nov-Dec;5(6):679-84.
The histology of Interleukin-2 induced tumour regression is presented. DBA/2 mice were injected simultaneously ip (intraperitoneally) and sc (subcutaneously) with 2 x 10(4) and 2 x 10(5) syngeneic SL2 lymphosarcoma cells, respectively. After treatment with 20,000 U IL-2 given ip at days 10-14, 50% of these mice survive. Histological analysis of the sc tumours showed that stagnation of blood flow and an occurrence of sudden massive necrosis were indicative of tumour regression. We hypothesize that peritoneal lymphocytes, activated by the ip tumour cells and IL-2, home in the sc tumour. There these activated lymphocytes produce lymphokines and trigger off other infiltrate cells to do similarly. This causes vascular leakage which leads to an increased intratumoural interstitial hydrostatic pressure. Subsequently circulatory obstruction and tumour necrosis occurs.
本文介绍了白细胞介素-2诱导肿瘤消退的组织学情况。将DBA/2小鼠分别经腹腔内（ip）和皮下（sc）同时注射2×10⁴和2×10⁵个同基因SL2淋巴肉瘤细胞。在第10 - 14天经腹腔给予20000 U白细胞介素-2治疗后，这些小鼠中有50%存活。对皮下肿瘤的组织学分析表明，血流停滞和突然出现的大量坏死是肿瘤消退的指征。我们推测，被腹腔内肿瘤细胞和白细胞介素-2激活的腹腔淋巴细胞迁移至皮下肿瘤。在那里，这些被激活的淋巴细胞产生淋巴因子，并促使其他浸润细胞也产生淋巴因子。这会导致血管渗漏，进而使肿瘤内间质流体静压升高。随后发生循环障碍和肿瘤坏死。
