期刊
BLOOD
卷 131, 期 10, 页码 1111-1121出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2017-08-802918
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资金
- National Science and Technology Major Project grant [2013ZX09301301]
- National Basic Research Program of China [2015CB553701]
- China Postdoctoral Science Foundation [2017M613317]
Effective vaccines against malaria caused by Plasmodium falciparum are still lacking, and the molecular mechanism of the host-parasite interaction is not fully understood. Here we demonstrate that the interaction of RAP2, a parasite-secreted rhoptry protein that functions in the parasitophorous vacuole formation stage of the invasion, and CD147 on the host erythrocyte is essential for erythrocyte invasion by P falciparum and is independent from all previously identified interactions involved. Importantly, the blockade of the CD147-RAP2 interaction by HP6H8, a humanized CD147 antibody, completely abolished the parasite invasion with both cure and preventative functions in a humanized mouse model. Together with its long half-life on human red blood cells and its safety profile in cynomolgus monkeys, HP6H8 is the first antibody that offers an advantageous approach by targeting a more conserved late-stage parasite ligand for preventing as well as treating severe malaria.
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