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布氏锥虫感染小鼠贫血的发病机制。

Pathogenesis of anemia in Trypanosoma brucei-infected mice.

作者信息

Amole B O, Clarkson A B, Shear H L

出版信息

Infect Immun. 1982 Jun;36(3):1060-8. doi: 10.1128/iai.36.3.1060-1068.1982.

Abstract

The pathogenesis of anemia was studied in trypanosome-infected mice. A strain of Trypanosoma brucei, TREU 667, was used which first produces an acute phase marked by waves of parasitemia. Erythrocytes from infected animals were coated with immunoglobulin M during or just before the waves of anemia and parasitological crises. Erythrocytes from normal animals could be sensitized with "precrisis" sera presumably containing antigen and antibody. These data suggest that anemia during the acute phase is due to sensitization of erythrocytes with immunoglobulin M-antigen complexes. The anemia is partially compensated by a strong erythropoietic response. The acute phase is followed by a chronic phase marked by a constant high parasitemia and immunosuppression. The less marked anemia occurring during this latter phase is due to hemodilution and perhaps a low but significant immune response to the parasites, which causes continuing erythrocyte sensitization by immunoglobulin M-antigen complexes.

摘要

对锥虫感染小鼠的贫血发病机制进行了研究。使用了一株布氏锥虫TREU 667,它首先会引发一个以寄生虫血症波动为特征的急性期。在贫血和寄生虫学危机出现期间或之前,感染动物的红细胞会被免疫球蛋白M包被。正常动物的红细胞可以用可能含有抗原和抗体的“危机前”血清进行致敏。这些数据表明,急性期的贫血是由于红细胞被免疫球蛋白M-抗原复合物致敏所致。强烈的红细胞生成反应可部分代偿这种贫血。急性期之后是慢性期,其特征是持续的高寄生虫血症和免疫抑制。后一阶段出现的不太明显的贫血是由于血液稀释,或许还由于对寄生虫的低水平但显著的免疫反应,这种反应导致红细胞持续被免疫球蛋白M-抗原复合物致敏。

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