Kongshavn P A, Shaw K, Ghadirian E, Ulczak O
Montreal General Hospital Research Institute, Quebec, Canada.
Infect Immun. 1990 Jun;58(6):1971-8. doi: 10.1128/iai.58.6.1971-1978.1990.
Previous studies have indicated that elimination of parasitemia in Trypanosoma musculi infection is brought about by immunoglobulin G2a antibodies, C3, and an effector cell. Experiments were designed to identify the putative effector cell by using several approaches. Infected C5-deficient or C5-sufficient mice treated with silica particles or given 900 rads of radiation 3 days earlier effectively eliminated trypanosomes following administration of immune plasma (IP). Silica-treated, noninfected mice given T. musculi preincubated with IP also cleared the parasites. Radiolabeling studies revealed that uptake of the cleared trypanosomes by the liver in normal mice was relatively low (24%) and fell only slightly (19%) in silica-treated mice. In contrast, uptake of radiolabeled sheep erythrocytes by the liver was normally much higher (47%) and fell drastically (7%) in silica-treated mice. Mice were then immunocompromised by 900 rads of radiation, silica particles, and anti-platelet serum combined before IP-sensitized trypanosomes were given. Leukocyte and platelet counts were both reduced by 95% and sheep erythrocyte uptake by the liver fell from 77 to 5%; however, greater than 99% of the injected trypanosomes were cleared in these mice and uptake of radiolabeled trypanosomes by the liver was similar to that of normal mice. Lastly, in anesthetized mice in which Kupffer cells were excluded surgically from the circulation, greater than 99% of the IP-sensitized trypanosomes disappeared rapidly from the blood. Only 7% of the radiolabel was found in the liver versus 60% in sham-operated mice. The results are interpreted as showing that hepatic Kupffer cells play a minor role in the immune elimination of T. musculi. Likewise, radiosensitive leukocytes and platelets are unlikely to be sole candidates for the putative effector cell that mediates a cure of murine trypanosomiasis.
先前的研究表明，在鼠锥虫感染中，寄生虫血症的消除是由免疫球蛋白G2a抗体、C3和一种效应细胞实现的。实验旨在通过几种方法来鉴定这种假定的效应细胞。在用二氧化硅颗粒处理或3天前接受900拉德辐射的C5缺陷或C5充足的感染小鼠中，给予免疫血浆（IP）后能有效消除锥虫。用IP预孵育鼠锥虫后给予经二氧化硅处理的未感染小鼠，这些小鼠也清除了寄生虫。放射性标记研究表明，正常小鼠肝脏对清除的锥虫的摄取相对较低（24%），在经二氧化硅处理的小鼠中仅略有下降（19%）。相比之下，肝脏对放射性标记的绵羊红细胞的正常摄取要高得多（47%），在经二氧化硅处理的小鼠中则大幅下降（7%）。然后，在给予IP致敏的锥虫之前，通过900拉德辐射、二氧化硅颗粒和抗血小板血清联合处理使小鼠免疫受损。白细胞和血小板计数均降低了95%，肝脏对绵羊红细胞的摄取从77%降至5%；然而，在这些小鼠中，超过99%的注射锥虫被清除，肝脏对放射性标记锥虫的摄取与正常小鼠相似。最后，在通过手术将库普弗细胞排除在循环之外的麻醉小鼠中，超过99%的IP致敏锥虫迅速从血液中消失。在肝脏中仅发现7%的放射性标记，而在假手术小鼠中为60%。结果表明，肝脏库普弗细胞在鼠锥虫的免疫消除中起次要作用。同样，对辐射敏感的白细胞和血小板不太可能是介导鼠锥虫病治愈的假定效应细胞的唯一候选者。
