Mauël J
Institute of Biochemistry, Epalinges, Switzerland.
J Leukoc Biol. 1990 Feb;47(2):187-93. doi: 10.1002/jlb.47.2.187.
Macrophages have different roles in Leishmania infections. They function as host-cells to the parasite, they present parasite antigens to the immune system, and they also act as effector cells responsible for parasite killing in the healing stages of the infection. Protein and carbohydrate ligands on the parasite surface, which interact with receptors on the macrophage membrane during phagocytosis, have been identified. Survival of Leishmania in its host cell requires a metabolic adaptation to the intracellular environment. The nutritional requirements of the microorganism must be satisfied and the deleterious effect of oxygen metabolites and of lysosomal hydrolases must be adequately counteracted. When a successful immune response develops, macrophages become activated and acquire the capacity to destroy the microorganism. Possible reasons why these mechanisms fail in certain individuals or experimental host-parasite combinations are discussed.
巨噬细胞在利什曼原虫感染中发挥着不同作用。它们作为寄生虫的宿主细胞，将寄生虫抗原呈递给免疫系统，并且在感染的愈合阶段还充当负责杀死寄生虫的效应细胞。已鉴定出寄生虫表面的蛋白质和碳水化合物配体，它们在吞噬作用期间与巨噬细胞膜上的受体相互作用。利什曼原虫在其宿主细胞中的存活需要对细胞内环境进行代谢适应。必须满足微生物的营养需求，并且必须充分抵消氧代谢产物和溶酶体水解酶的有害作用。当成功的免疫反应产生时，巨噬细胞被激活并获得破坏微生物的能力。本文讨论了这些机制在某些个体或实验宿主 - 寄生虫组合中失败的可能原因。
