Haplotype of non-synonymous mutations within IL-23R is associated with susceptibility to severe malaria anemia in a P. falciparum holoendemic transmission area...
|dc.contributor.author||Munde, Elly O|
|dc.contributor.author||Okeyo, Winnie A|
|dc.contributor.author||Ong’echa, John M|
|dc.contributor.author||Perkins, Douglas J|
|dc.description.abstract||Background Improved understanding of the molecular mechanisms involved in pediatric severe malarial anemia (SMA) pathogenesis is a crucial step in the design of novel therapeutics. Identification of host genetic susceptibility factors in immune regulatory genes offers an important tool for deciphering malaria pathogenesis. The IL-23/IL-17 immune pathway is important for both immunity and erythropoiesis via its effects through IL-23 receptors (IL-23R). However, the impact of IL-23R variants on SMA has not been fully elucidated. Methods Since variation within the coding region of IL-23R may influence the pathogenesis of SMA, the association between IL-23R rs1884444 (G/T), rs7530511 (C/T), and SMA (Hb< 6.0 g/dL) was examined in children (n= 369, aged 6–36 months) with P. falciparum malaria in a holoendemic P. falciparum transmission area. Results Logistic …||en_US|
|dc.title||Haplotype of non-synonymous mutations within IL-23R is associated with susceptibility to severe malaria anemia in a P. falciparum holoendemic transmission area...||en_US|
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