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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 Fcgamma receptor II (FcgammaRII). A single amino acid substitution at position 131 in FcgammaRIIa is critical in the binding of human IgG subclasses. The hypothesis that the FcgammaRIIa-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 FcgammaRIIa-Arg/Arg131 genotype were significantly less likely to be at risk for high-density falciparum infection, compared with infants with the FcgammaRIIa-His/Arg131 genotype (adjusted odds ratio, 0.278; 95% confidence interval, 0.123-0.627; P=.0021). This finding supports the hypothesis.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Fcγ Receptor IIa (CD32) Polymorphism Is Associated with Protection of Infants against High‐Density<i>Plasmodium falciparum</i>Infection. VII. Asembo Bay Cohort Project

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