Fauve R M, Hevin B, Jacob H, Gaillard J A, Jacob F
Proc Natl Acad Sci U S A. 1974 Oct;71(10):4052-6. doi: 10.1073/pnas.71.10.4052.
Development of teratocarcinoma does not impair immunization of mice against Listeria monocytogenes. Endotoxin injection a short time before tumor cell inoculation allows the growth of teratocarcinoma in non syngenic mice despite immune stimulation. In contrast with this absence of impaired systematic immunity, teratocarcinoma cells were found to repulse macrophages in vitro. This effect on macrophages was also found with three other malignant cells and with trophoblast cells. In vivo, teratocarcinoma cells were found to impair local inflammation. These cells and other malignant cells are able to produce a compound(s) of molecular weight between 10(3) and 10(4), which prevents inflammatory reaction. These results suggest that mouse teratocarcinomas and other tumors by-pass the host immunological system of surveillance by at least two mechanisms: a direct toxic effect on macrophages and the release of an inhibitor of inflammation. The possible relations between these properties of malignant cells and physiological functions of trophoblast are discussed.
畸胎癌的发展并不损害小鼠针对单核细胞增生李斯特菌的免疫。在接种肿瘤细胞前短时间注射内毒素,尽管有免疫刺激,仍可使畸胎癌在非同基因小鼠体内生长。与全身免疫未受损相反,发现畸胎癌细胞在体外排斥巨噬细胞。另外三种恶性细胞和滋养层细胞对巨噬细胞也有这种作用。在体内,发现畸胎癌细胞会损害局部炎症。这些细胞和其他恶性细胞能够产生一种分子量在10³至10⁴之间的化合物,该化合物可阻止炎症反应。这些结果表明,小鼠畸胎癌和其他肿瘤至少通过两种机制绕过宿主的免疫监视系统:对巨噬细胞的直接毒性作用和炎症抑制剂的释放。文中还讨论了恶性细胞的这些特性与滋养层生理功能之间的可能关系。