ArticleBMC infectious diseases2017
Haplotype of non-synonymous mutations within IL-23R is associated with susceptibility to severe malaria anemia in a P. falciparum holoendemic transmission area of Kenya.
Article in BMC infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Plasma Soluble Progenitor Cell Receptors as Biomarkers for Severe Anemia Among Malaria-Infected Pediatrics: A Prospective Study in Ghana.Health science reports · 2025Article
- Genetics of cerebral malaria: pathogenesis, biomarkers and emerging therapeutic interventions.Cell & bioscience · 2022Review
- Nonsynonymous amino acid changes in the α-chain of complement component 5 influence longitudinal susceptibility toFrontiers in genetics · 2022Article
- Haematological abnormalities in children with sickle cell disease and non-severe malaria infection in western Kenya.BMC infectious diseases · 2021Article
- Human genetics and malaria resistance.Human genetics · 2020Review
- Article
- Molecular basis of reduced LAIR1 expression in childhood severe malarial anaemia: Implications for leukocyte inhibitory signalling.EBioMedicine · 2019Article
- Eryptosis of non-parasitized erythrocytes is related to anemia in Plasmodium berghei low parasitema malaria of Wistar rats.Parasitology research · 2019Article
- Molecular and Functional Characterization of Fcγ Receptor IIIb-Ligand Interaction: Implications for Neutrophil-Mediated Immune Mechanisms in Malaria.Infection and immunity · 2018Article
- Novel genetic polymorphisms associated with severe malaria and under selective pressure in North-eastern Tanzania.PLoS genetics · 2018Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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Abstract
backgroundImproved 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.
methodsSince 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.
resultsLogistic regression analysis, controlling for confounding factor of anemia, revealed that individual genotypes of IL-23R rs1884444 (G/T) [GT; OR = 1.34, 95% CI = 0.78-2.31, P = 0.304 and TT; OR = 2.02, 95% CI = 0.53-7.74, P = 0.286] and IL-23R rs7530511 (C/T) [CT; OR = 2.6, 95% CI = 0.59-11.86, P = 0.202 and TT; OR = 1.66, 95% CI = 0.84-3.27, P = 0.142] were not associated with susceptibility to SMA. However, carriage of IL-23R rs1884444T/rs7530511T (TT) haplotype, consisting of both mutant alleles, was associated with increased susceptibility to SMA (OR = 1.12, 95% CI = 1.07-4.19, P = 0.030).
conclusionResults presented here demonstrate that a haplotype of non-synonymous IL-23R variants increase susceptibility to SMA in children of a holoendemic P. falciparum transmission area.
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