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CD36 deficiency protects against malarial anaemia in children by reducing Plasmodium falciparum‐infected red blood cell adherence to vascular endothelium

Summary Objective  CD36 is a receptor that occurs on the surface of activated immune cells, vascular endothelial cells and participates in phagocytosis and lipid metabolism. CD36 is known to be the major endothelial receptor molecule for field isolates of Plasmodium falciparum. A T1264G mutation in...

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Published in:Tropical medicine & international health 2009-07, Vol.14 (7), p.810-816
Main Authors: Chilongola, Jaffu, Balthazary, Sakurani, Mpina, Maximillian, Mhando, Martin, Mbugi, Erasto
Format: Article
Language:English
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Summary:Summary Objective  CD36 is a receptor that occurs on the surface of activated immune cells, vascular endothelial cells and participates in phagocytosis and lipid metabolism. CD36 is known to be the major endothelial receptor molecule for field isolates of Plasmodium falciparum. A T1264G mutation in exon X of the gene leads to deficiency of CD36. This study aimed at determining associations between CD36 deficiency, P. falciparum in vitro adherence on purified CD36 and anaemia among children in an endemic area. Methods  Genotypes were determined by nested polymerase chain reaction of isolated DNA from filter blood spots followed by Restriction Fragment Length Polymorphism (RFLP). Plasmodium falciparum adherence assays were performed on immobilized purified CD36. Results  The data indicate that CD36 is an important cytoadherence receptor that mediates adherence to most P. falciparum field isolates. Our findings also suggest that mutations causing CD36 deficiency may confer significant protection against malarial anaemia (MA) in children (χ2 = 8.58, P 
ISSN:1360-2276
1365-3156
DOI:10.1111/j.1365-3156.2009.02298.x