Hoover D L, Nacy C A
J Immunol. 1984 Mar;132(3):1487-93.
Resident peritoneal macrophages and macrophages elicited by injection of C3H/HeN mice with sterile inflammatory agents were exposed to amastigotes of Leishmania tropica in vitro and treated with lymphokines. Resident macrophages developed the capacity to kill intracellular parasites; microbicidal activity of activated resident cells ranged between 60 and 80%. In contrast, inflammatory macrophages responded poorly to lymphokines for intracellular killing of amastigotes; microbicidal activity of cells elicited with chronic inflammatory agents ranged between 0 and 45%. Defective intracellular killing of L. tropica by inflammatory macrophages was independent of the agent used to elicit the cells, but was clearly associated with the number of immature macrophages in the population. That intracellular killing capacity may reflect the presence of a killing mechanism in tissue-derived cells that is not yet developed in undifferentiated macrophages is supported by studies with peripheral blood monocytes: these cells were also incapable of eliminating intracellular amastigotes in the presence of potent activating factors. These observations on inflammatory macrophage interactions with amastigotes may provide important insights into the chronic nature of leishmanial disease.
将无菌炎性因子注射到C3H/HeN小鼠体内诱导产生的腹膜巨噬细胞和炎性巨噬细胞，在体外与热带利什曼原虫无鞭毛体接触，并接受淋巴因子处理。驻留巨噬细胞获得了杀死细胞内寄生虫的能力；活化的驻留细胞的杀菌活性在60%至80%之间。相比之下，炎性巨噬细胞对淋巴因子介导的细胞内无鞭毛体杀伤反应较差；由慢性炎性因子诱导产生的细胞的杀菌活性在0%至45%之间。炎性巨噬细胞对热带利什曼原虫细胞内杀伤缺陷与诱导细胞所用的因子无关，但明显与群体中未成熟巨噬细胞的数量有关。外周血单核细胞的研究支持了细胞内杀伤能力可能反映了组织来源细胞中存在一种未分化巨噬细胞尚未发育的杀伤机制：在存在强效激活因子的情况下，这些细胞也无法清除细胞内的无鞭毛体。这些关于炎性巨噬细胞与无鞭毛体相互作用的观察结果，可能为利什曼病的慢性本质提供重要见解。
