Gilks C F, Walliker D, Newbold C I
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Headington, Oxford.
Parasite Immunol. 1990 Jan;12(1):45-64. doi: 10.1111/j.1365-3024.1990.tb00935.x.
We describe here a rodent malaria model using cloned lines of Plasmodium chabaudi chabaudi in inbred CBA/Ca mice that exhibits both clonal antigenic variation in late stage-specific surface antigens, and deep vascular schizogony in the liver. We show that both these features are modulated by the spleen, and that surface antigen expression is crucially involved in the sequestering phenotype. Surface antigens are variant in chronic infection, and host protective immune responses can distinguish between these variants. Splenectomy abolishes this difference. The acute infection with non-sequestering cloned lines is kinetically indistinguishable from sequestering clones, but parasites unable to express variant sequestration-associated antigen do not form a chronic recrudescing infection. Another clone, able to re-express this antigen in the presence of the spleen, undergoes typical chronic recrudescence. In this model, the biological significance of sequestration-associated variant antigen seems to enable the establishment of chronic infection in the presence of a primed spleen.
我们在此描述一种啮齿动物疟疾模型，该模型使用近交系CBA/Ca小鼠体内的约氏疟原虫克隆株，其在晚期特异性表面抗原中表现出克隆抗原变异，并且在肝脏中存在深层血管内裂体增殖。我们发现这两个特征均受脾脏调节，并且表面抗原表达与滞留表型密切相关。表面抗原在慢性感染中具有变异性，宿主的保护性免疫反应能够区分这些变异体。脾切除消除了这种差异。非滞留克隆株的急性感染在动力学上与滞留克隆株无法区分，但无法表达与滞留相关的变异抗原的寄生虫不会形成慢性复发性感染。另一个克隆株在脾脏存在的情况下能够重新表达这种抗原，会经历典型的慢性复发。在这个模型中，与滞留相关的变异抗原的生物学意义似乎是在已致敏的脾脏存在的情况下能够建立慢性感染。
