The apicomplexan parasite Babesia microti is the primary agent of human babesiosis, a malaria-like illness and potentially fatal tick-borne disease. Unlike its close relatives, the agents of human malaria, B. microti develops within human and mouse red blood cells in the absence of a parasitophorous vacuole, and its secreted antigens lack trafficking motifs found in malarial secreted antigens. Here, we show that after invasion of erythrocytes, B. microti undergoes a major morphogenic change during which it produces an interlacement of vesicles (IOV); the IOV system extends from the plasma membrane of the parasite into the cytoplasm of the host erythrocyte. We developed antibodies against two immunodominant antigens of the parasite and used them in cell fractionation studies and fluorescence and immunoelectron microscopy analyses to monitor the mode of secretion of B. microti antigens. These analyses demonstrate that the IOV system serves as a major export mechanism for important antigens of B. microti and represents a novel mechanism for delivery of parasite effectors into the host by this apicomplexan parasite.

中文翻译：

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人类病原体小巴贝虫（Babesia microti）囊泡介导的抗原输出的证据。

apicomplexan寄生虫小巴贝虫是人类巴贝虫病的主要病原体，这是一种类似于疟疾的疾病，可能是致命的tick传播疾病。与它的近亲不同，人疟疾的病原体在没有寄生虫液泡的情况下在人和小鼠的红细胞内发展，其分泌的抗原缺乏在疟疾分泌的抗原中发现的运输基序。在这里，我们表明，红细胞入侵后，小芽孢杆菌经历主要的形态发生变化，在此过程中会产生囊泡交错（IOV）；IOV系统从寄生虫的质膜延伸到宿主红细胞的细胞质中。我们开发了针对该寄生虫的两种免疫优势抗原的抗体，并将其用于细胞分级研究以及荧光和免疫电子显微镜分析，以监测B. microti抗原的分泌模式。这些分析表明，IOV系统充当了微小芽孢杆菌重要抗原的主要输出机制，并且代表了一种新的机制，可通过这种apicomplexan寄生虫将寄生效应子传递到宿主中。