ArticleScientific reports2017
A Functional IL22 Polymorphism (rs2227473) Is Associated with Predisposition to Childhood Cerebral Malaria.
Article in Scientific reports, 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, 18 citations in OpenAlex.
- Cytokine gene polymorphisms implicated in the pathogenesis ofFrontiers in immunology · 2024Review
- Association between interleukin-27 gene polymorphisms andInnate immunity · 2023Article
- Review
- Identification of genetic variants of the IL-22 gene in association with an altered risk of COPD susceptibility.The clinical respiratory journal · 2022Article
- Genetics of cerebral malaria: pathogenesis, biomarkers and emerging therapeutic interventions.Cell & bioscience · 2022Review
- The good and the bad about separation anxiety: roles of IL-22 and IL-22BP in liver pathologies.Seminars in immunopathology · 2021Review
- Data-driven malaria prevalence prediction in large densely populated urban holoendemic sub-Saharan West Africa.Scientific reports · 2020Article
- Pathophysiology and neurologic sequelae of cerebral malaria.Malaria journal · 2020Review
- Interleukin-22 Polymorphisms inMediators of inflammation · 2020Article
- Evaluation of single nucleotide polymorphism in interleukin 22 (IL-22) gene and its association with chronic hepatitis B infection.Gastroenterology and hepatology from bed to bench · 2019Article
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Authors and funding
18 authors at 8 institutions in 4 countries.
Funding
Abstract
Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection. This encephalopathy is characterized by coma and is thought to result from mechanical microvessel obstruction and an excessive activation of immune cells leading to pathological inflammation and blood-brain barrier alterations. IL-22 contributes to both chronic inflammatory and infectious diseases, and may have protective or pathogenic effects, depending on the tissue and disease state. We evaluated whether polymorphisms (n = 46) of IL22 and IL22RA2 were associated with CM in children from Nigeria and Mali. Two SNPs of IL22, rs1012356 (P = 0.016, OR = 2.12) and rs2227476 (P = 0.007, OR = 2.08) were independently associated with CM in a sample of 115 Nigerian children with CM and 160 controls. The association with rs2227476 (P = 0.01) was replicated in 240 nuclear families with one affected child from Mali. SNP rs2227473, in linkage disequilibrium with rs2227476, was also associated with CM in the combined cohort for these two populations, (P = 0.004, OR = 1.55). SNP rs2227473 is located within a putative binding site for the aryl hydrocarbon receptor, a master regulator of IL-22 production. Individuals carrying the aggravating T allele of rs2227473 produced significantly more IL-22 than those without this allele. Overall, these findings suggest that IL-22 is involved in the pathogenesis of CM.
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