原创力文档a role for fetal hemoglobin and maternal immune igg in infant resistance to plasmodium falciparum malaria胎儿血红蛋白的作用和产妇婴儿抗恶性疟原虫疟疾免疫免疫球蛋白.pdfVIP
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a role for fetal hemoglobin and maternal immune igg in infant resistance to plasmodium falciparum malaria胎儿血红蛋白的作用和产妇婴儿抗恶性疟原虫疟疾免疫免疫球蛋白
A Role for Fetal Hemoglobin and Maternal Immune IgG
in Infant Resistance to Plasmodium falciparum Malaria
1 1 1 1
Chanaki Amaratunga , Tatiana M. Lopera-Mesa , Nathaniel J. Brittain , Rushina Cholera , Takayuki
2 3 4 1
Arie , Hisashi Fujioka , Jeffrey R. Keefer , Rick M. Fairhurst *
1 Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of
America, 2 Department of Physics and Electronics, School of Engineering, Osaka Prefecture University, Osaka, Japan, 3 Department of Pharmacology, Case Western
Reserve University, Cleveland, Ohio, United States of America, 4 Division of Pediatric Hematology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore,
Maryland, United States of America
Abstract
Background: In Africa, infant susceptibility to Plasmodium falciparum malaria increases substantially as fetal hemoglobin
(HbF) and maternal immune IgG disappear from circulation. During the first few months of life, however, resistance to
malaria is evidenced by extremely low parasitemias, the absence of fever, and the almost complete lack of severe disease.
This resistance has previously been attributed in part to poor parasite growth in HbF-containing red blood cells (RBCs). A
specific role for maternal immune IgG in infant resistance to malaria has been hypothesized but not yet identified.
Methods and Findings: We found that P. falciparum parasites invade and develop normally in fetal (cord blood, CB) RBCs,
which contain up to 95% HbF. However, these parasitized CB RBCs are impaired in their binding to human microvas
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