Nogueira N, Chaplan S, Cohn Z
J Exp Med. 1980 Aug 1;152(2):447-51. doi: 10.1084/jem.152.2.447.
Blood form trypomastigotes of the Y and CL strains of Trypanosoma cruzi were tested for their ability to enter and infect mouse peritoneal macrophages. Both strains failed to enter macrophages in appreciable numbers, whereas metacyclic trypomastigotes purified from acellular cultures were ingested with ease. Macrophage parasitization was enhanced manyfold after the removal of an antiphagocytic substance by trypsinization. This occurred without modification of parasite viability. Opsonization with hyperimmune mouse serum also enhanced the uptake of blood form trypomastigotes by macrophages. This effect was mediated by the macrophage Fc receptor. The effects of serum and trypsinization were additive at high parasite:cell ratios. Neither trypsin-mediated nor antibody-dependent opsonization of the organisms modified the fate of either strain within resident macrophages. However, lymphokine-activated macrophages were capable of destroying both strains, and antibody opsonization further enhanced this process.
对克氏锥虫Y株和CL株的血液型锥鞭毛体进入并感染小鼠腹腔巨噬细胞的能力进行了测试。两种菌株均未能大量进入巨噬细胞，而从无细胞培养物中纯化的循环后期锥鞭毛体则很容易被摄取。通过胰蛋白酶处理去除抗吞噬物质后，巨噬细胞的寄生作用增强了许多倍。这一过程中寄生虫的活力未发生改变。用超免疫小鼠血清进行调理也增强了巨噬细胞对血液型锥鞭毛体的摄取。这种作用是由巨噬细胞Fc受体介导的。在高寄生虫与细胞比例时，血清和胰蛋白酶处理的作用是相加的。胰蛋白酶介导的或抗体依赖性的生物体调理均未改变两种菌株在驻留巨噬细胞内的命运。然而，淋巴因子激活的巨噬细胞能够破坏这两种菌株，抗体调理进一步增强了这一过程。
