Chang K P, Chiao J W
Proc Natl Acad Sci U S A. 1981 Nov;78(11):7083-7. doi: 10.1073/pnas.78.11.7083.
Leishmania donovani, an intracellular protozoan, causes kala-azar by parasitizing the macrophages of its mammalian host. Outbred NCS and CD-1 mice develop immunity to this parasite. This immunity was demonstrable when supernatant fluids from cultured splenic lymphocytes were added to infected macrophages. Only the lymphokine preparations from infected mice showed significant leishmanicidal activity. Mice receiving multiple inocula were more potent producers of leishmanicidal lymphokines than were those receiving single inocula. The expression of leishmanicidal activity in our system required continuous presence of the lymphokine preparation and was independent of trypsin- or neuraminidase-sensitive receptors of the macrophages. Light and electron microscopy revealed that, in the presence of lymphokines, macrophages appeared to be "activated," and intracellular leishmanias developed specific subcellular lesions in the kinetoplast-mitochondria. A time-course study showed that cultivation of the lymphocytes for 1 1/2 days completed the release of their leishmanicidal lymphokines which were heat-labile molecules larger than 50,000 daltons.
杜氏利什曼原虫是一种细胞内原生动物，通过寄生于其哺乳动物宿主的巨噬细胞引起黑热病。远交群NCS和CD-1小鼠对这种寄生虫产生免疫力。当将培养的脾淋巴细胞的上清液添加到感染的巨噬细胞中时，这种免疫力就可以得到证明。只有来自感染小鼠的淋巴因子制剂显示出显著的杀利什曼原虫活性。接受多次接种的小鼠比接受单次接种的小鼠更能有效地产生杀利什曼原虫淋巴因子。在我们的系统中，杀利什曼原虫活性的表达需要淋巴因子制剂的持续存在，并且与巨噬细胞的胰蛋白酶或神经氨酸酶敏感受体无关。光学显微镜和电子显微镜显示，在淋巴因子存在的情况下，巨噬细胞似乎被“激活”，并且细胞内利什曼原虫在动基体-线粒体中出现特定的亚细胞病变。一项时间进程研究表明，淋巴细胞培养1.5天可完成其杀利什曼原虫淋巴因子的释放，这些淋巴因子是大于50,000道尔顿的热不稳定分子。
