Plasmodium falciparum rhoptry protein RSP2 triggers destruction of the erythroid lineage
Plasmodium falciparum rhoptry protein RSP2 triggers destruction of the erythroid lineage
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DOI：
10.1182/blood-2005-04-1574
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发表时间：
2005-11-15
期刊：
影响因子：
20.3
通讯作者：
Gysin, J
中科院分区：
文献类型：
--
作者：
Layez, C;Nogueira, P;Gysin, J
红细胞的破坏和红细胞生成的缺陷是严重恶性疟原虫疟疾中最常见的发病原因。尽管进行了广泛的研究，但涉及的分子机制仍不清楚。我们在这里表明，第一次，标记与寄生虫棒状蛋白环表面蛋白2（RSP2）不限于正常红细胞的表面，如以前报道的，但它延伸到贫血疟疾患者骨髓中的红系前体细胞。来自严重贫血患者的单克隆小鼠抗体和人血清与RSP2标记的红细胞反应，通过体外吞噬作用和补体激活诱导细胞破坏。我们的观察揭示了一种新的寄生虫机制，与疟疾患者正常红细胞的破坏和红细胞生成障碍有关。这些数据表明，用RSP2标记宿主细胞可能会引发恶性疟疾的贫血。
The destruction of erythrocytes and defects in erythropoiesis are among the most frequently observed causes of morbidity in severe Plasmodium falciparum malaria. The molecular mechanisms involved remain unclear, despite extensive investigation. We show here, for the first time, that tagging with the parasite rhoptry protein ring surface protein 2 (RSP2) is not restricted to the surfaces of normal erythrocytes, as previously reported, but that it extends to erythroid precursor cells in the bone marrow of anemic malaria patients. Monoclonal mouse antibodies and human sera from patients with severe anemia, reacting with RSP2-tagged erythrocytes, induced cell destruction by phagocytosis and complement activation in vitro. Our observations reveal a new parasite mechanism implicated in the destruction of normal erythrocytes and probably dyserythropoiesis in malaria patients. These data suggest that the tagging of host cells with RSP2 may trigger anemia in falciparum malaria.