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恶性疟原虫感染的地中海贫血红细胞的细胞黏附及花结形成的改变。

Alteration in cytoadherence and rosetting of Plasmodium falciparum-infected thalassemic red blood cells.

作者信息

Udomsangpetch R, Sueblinvong T, Pattanapanyasat K, Dharmkrong-at A, Kittikalayawong A, Webster H K

机构信息

Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok, Thailand.

出版信息

Blood. 1993 Dec 15;82(12):3752-9.

PMID:8260712
Abstract

Hemoglobinopathies have a protective role in malaria that appears to be related to alterations in red blood cell (RBC) properties. Thalassemic RBCs infected with Plasmodium falciparum showed greatly reduced cytoadherence and rosetting properties as well as impaired growth and multiplication. A significant decrease in the levels of falciparum antigens associated with the membrane of infected beta-thalassemic RBCs was observed at trophozoite/schizont stage, but not young ring stage. This reduction was shown when a cytoadherence inhibitory monoclonal antibody, but not a noninhibitory pooled immune serum, was used. These observations suggest that protection against malaria in thalassemia is caused by both reduced parasitemias and altered adherence properties of the infected thalassemic RBCs that promote enhanced clearance of the parasite from the circulation.

摘要

血红蛋白病在疟疾中具有保护作用,这似乎与红细胞(RBC)特性的改变有关。感染恶性疟原虫的地中海贫血红细胞表现出细胞黏附性和花结形成特性大大降低,以及生长和繁殖受损。在滋养体/裂殖体阶段观察到与受感染的β地中海贫血红细胞膜相关的恶性疟原虫抗原水平显著下降,但在早期环状体阶段未观察到。当使用细胞黏附抑制性单克隆抗体而非非抑制性混合免疫血清时,出现了这种降低。这些观察结果表明,地中海贫血对疟疾的保护作用是由寄生虫血症降低以及受感染的地中海贫血红细胞黏附特性改变共同引起的,后者促进了寄生虫从循环中清除。

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