DeGraves F J, Cox H W
J Parasitol. 1983 Apr;69(2):262-6.
Anemia, thrombocytopenia and reduction in parasitemia in P. chabaudi infection of rats were associated with appearance in blood of soluble immune complexes, immunoconglutinin (IK), and by reductions in titers of lytic complement. With reduction of parasitemia to subpatent levels, anemia, but not thrombocytopenia, persisted and erythrocyte counts did not return to preinfection levels for several weeks. This chronic anemia was accompanied by elevated amounts of soluble immune complex, depressed titers of lytic complement and persistence of IK. Evidence was presented indicating that the infections of the rats persisted in a chronic form. It was thus indicated that immune interactions, related to anemia and clearance of parasitemia, persisted in absence of microscopically evident parasitemia, and may have been in part responsible for the persistent anemia. Based on the evidence cited, it is suggested that complement-fixing immune complexes attach to blood cells, infected as well as uninfected, and that these cells are sequestered and phagocytized in the spleen after immunoconglutination by IK. It is also suggested that this interaction continued after the clearance of patent parasitemia and accounted for the persistence of anemia in the chronic phase of infection.
在大鼠感染查巴迪疟原虫的过程中，贫血、血小板减少以及疟原虫血症的降低与血液中可溶性免疫复合物、免疫黏附素（IK）的出现以及溶细胞补体滴度的降低有关。随着疟原虫血症降至亚临床水平，贫血持续存在，而血小板减少不再出现，红细胞计数在数周内未恢复到感染前水平。这种慢性贫血伴随着可溶性免疫复合物量的增加、溶细胞补体滴度的降低以及IK的持续存在。有证据表明大鼠感染以慢性形式持续存在。因此表明，在没有显微镜下明显疟原虫血症的情况下，与贫血和疟原虫血症清除相关的免疫相互作用持续存在，并且可能部分导致了持续性贫血。根据所引用的证据，提示补体结合免疫复合物附着于血细胞，包括感染和未感染的血细胞，并且这些细胞在被IK免疫黏附后在脾脏中被隔离和吞噬。还提示这种相互作用在显性疟原虫血症清除后仍持续存在，并解释了感染慢性期贫血的持续存在。
