| dc.description.abstract | An understanding of the immunogenetic basis of naturally acquired immunity to Plasmodium
falciparum infection would aid in the designing of a rationally based malaria vaccine.
Variants within the Fc gamma receptors (FcγRs) mediate immunity through engagement of
immunoglobulin G and other immune mediators, such as gamma interferon (IFN-γ), resulting
in erythrophagocytosis and production of inflammatory cytokines in severe malarial anemia
(SMA). The Toll-like receptors (TLRs) trigger transcription of proinflammatory cytokines and
induce adaptive immune responses. Therefore, these receptors may condition malaria
disease pathogenesis through alteration in adaptive and innate immune responses. To
further delineate the impacts of FcγRIIIA and TLR9 in SMA pathogenesis, the associations
between FcγRIIIA− 176F/V and TLR9− 1237T/C variants, SMA (hemoglobin [Hb]< 6.0 g/dl … | en_US |
