Barnwell J W, Howard R J, Miller L H
J Immunol. 1982 Jan;128(1):224-6.
Variant antigens are present on the surface of Plasmodium knowlesi malaria-infected erythrocytes as detected by the schizont-infected cell agglutination (SICA) assay. We found that parasitized erythrocytes passaged in splenectomized monkeys did not agglutinate with immune sera. On the first passage from intact to splenectomized monkeys, the SICA titers decreased 4- to 16-fold; after the second and subsequent passages in splenectomized monkeys, the infected cells became nonagglutinable to all sera tested, including sera from animals infected with the nonagglutinating parasites. This loss of agglutinability could have resulted from selection of a genetically distinct subpopulation of the original parasites or the ability of the original parasites to alter their phenotypic expression. We have designated the new nonagglutinable phenotype, SICA [-], and the agglutinable phenotype, SICA [+]. The loss of agglutinability indicates that the variant antigen normally expressed on the erythrocyte membrane of infected cells is altered or absent. Because SICA [-] parasites developed in the absence of the spleen, the major organ of host defense against malaria, then this organ may in some manner influence or modulate antigenic expression in P. knowlesi and possibly other malaria parasites.
通过裂殖体感染细胞凝集(SICA)试验检测发现,变异抗原存在于诺氏疟原虫感染的红细胞表面。我们发现,在脾切除的猴子体内传代的被寄生红细胞不会与免疫血清发生凝集。从完整的猴子到脾切除的猴子进行首次传代时,SICA滴度下降了4至16倍;在脾切除的猴子体内进行第二次及后续传代后,感染的细胞对所有测试血清均无凝集反应,包括来自感染了非凝集性寄生虫的动物的血清。这种凝集性的丧失可能是由于选择了原始寄生虫的一个基因上不同的亚群,或者是原始寄生虫改变其表型表达的能力所致。我们将新的非凝集性表型命名为SICA [-],将凝集性表型命名为SICA [+]。凝集性的丧失表明,正常情况下在感染细胞的红细胞膜上表达的变异抗原发生了改变或缺失。由于SICA [-]寄生虫是在作为宿主抵御疟疾的主要器官的脾脏缺失的情况下产生的,那么这个器官可能以某种方式影响或调节诺氏疟原虫以及可能其他疟原虫的抗原表达。