We observed a significant increase in the production of anti-MSP-119 IgG antibody

in normal and heterozygous children during the 12 months of follow-up, but see more not in homozygous mutants. Normal children had a significantly lower malaria incidence rate compared to other genotypes (χ2 = 115.59; P < 0.01). We conclude that the presence of the c.1264 T>G mutation that leads to CD36 deficiency is closely associated with reduced IgG production and higher malaria incidence. It is most likely that deficiency of CD36 which is known to modulate dendritic cell function suppresses the production of protective IgG antibodies directed to Plasmodium falciparum MSP-119 antigen, which predisposes to the acquisition of clinical malaria in children. Adhesion molecules are proteins located on the cell surface, involved in binding

with other cells or with the extracellular matrix in a process called cytoadherence, and which occurs as a result of the interaction between parasite ligands and host receptors. FDA-approved Drug Library high throughput Cytoadherence of infected erythrocytes containing late developmental stages of the malaria parasites (trophozoites and schizonts) to the endothelium of capillaries and venules is characteristic of Plasmodium falciparum infections [1]. Cytoadherence is an important mechanism in the pathogenesis of malaria. Polymorphisms in more than 30 human genes determining the immune response have been associated with susceptibility to malaria [2], particularly in genes

involved in cell adhesion and immunity. Cell adhesion molecules (CAM) have been identified as receptors for infected red blood cell and are associated with susceptibility to malaria. The adhesion molecules include CD36, intercellular adhesion molecule 1 (ICAM-1, CD54), platelet/endothelial cell adhesion molecule1 (PECAM-1, CD31), vascular cell adhesion molecule1 (VCAM-1), thrombospondin, E-selectin, P-selectin and chondrotin sulphate A [3]. Most P. falciparum antigens bind to CD36 molecules, which Gefitinib concentration are thus considered to be the major endothelial receptors for sequestration [4]. Mutations in the CD36 gene may, therefore, influence the outcome of malaria. CD36 is an 88-kDa member of the class B scavenger receptor family of cell surface glycoproteins. CD36 is broadly expressed on monocytes, macrophages, dendritic cells, fat cells, muscle cells, capillary endothelial cells and platelets [5]. CD36 acts as a facilitator of fatty acid uptake and is a receptor for a wide range of ligands including collagen, thrombospondin, anionic phospholipids, oxidized low density lipoprotein and erythrocytes parasitized with P. falciparum [6–8], and participate in macrophage fusion induced by IL-4 cytokines [9]. In vitro studies carried out by Urban and colleagues revealed that P.