Show simple item record

dc.contributor.authorMunde, Elly O
dc.contributor.authorRaballah, Evans
dc.contributor.authorOkeyo, Winnie A
dc.contributor.authorOng’echa, John M
dc.contributor.authorPerkins, Douglas J
dc.contributor.authorOuma, Collins
dc.date.accessioned2018-01-19T13:38:05Z
dc.date.available2018-01-19T13:38:05Z
dc.date.issued2017-04-20
dc.identifier.urihttps://repository.maseno.ac.ke/handle/123456789/155
dc.description.abstractBackground 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.publisherBioMed Centralen_US
dc.titleHaplotype of non-synonymous mutations within IL-23R is associated with susceptibility to severe malaria anemia in a P. falciparum holoendemic transmission area...en_US
dc.typeArticleen_US


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record