Fcγ Receptor IIa (CD32) Polymorphism Is Associated with Protection of Infants against High‐DensityPlasmodium falciparumInfection. VII. Asembo Bay Cohort Project

Open Access
Publisher Website
Google Scholar
Abstract
In vitro studies have shown that inhibition of Plasmodium falciparum blood-stage parasite growth by antibody-dependent cellular inhibition is mediated by cooperation between malaria-specific IgG1 and IgG3, but not IgG2, and monocytes via the Fcγ receptor II (FcγRII). A single amino acid substitution at position 131 in FcγRIIa is critical in the binding of human IgG subclasses. The hypothesis that the FcγRIIa-Arg/Arg131 genotype, which does not bind to IgG2, is a host genetic factor for protection against high-density P. falciparum infection was tested. One hundred eighty-two infants from a large community-based birth cohort study in western Kenya were selected for an unmatched case-control study. Results showed that the infants with the FcγRIIa-Arg/Arg131 genotype were significantly less likely to be at risk for high-density falciparum infection, compared with infants with the FcγRIIa-His/Arg131 genotype (adjusted odds ratio, 0.278; 95% confidence interval, 0.123–0.627; P=.0021). This finding supports the hypothesis

This publication has 0 references indexed in Scilit: