ArticleMalaria journal2026
Association of interleukin-33 gene polymorphisms with susceptibility to Plasmodium falciparum infection.
Article in Malaria journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHost immune genetic variation contributes to inter-individual differences in susceptibility to Plasmodium falciparum malaria and parasite-burden response. Interleukin-33 (IL-33), an IL-1 family alarmin signaling through ST2, regulates innate and adaptive immune responses during infection. Although IL-33/ST2 signaling has been implicated in malaria-related immune regulation, the contribution of IL-33 genetic variation to human P. falciparum susceptibility remains insufficiently defined.
methodsThis case-control study included 250 individuals with active P. falciparum malaria and 200 healthy controls from the Jazan region of Southwestern Saudi Arabia. Thirteen IL-33 SNPs were genotyped, and associations were evaluated in relation to malaria susceptibility, parasite-density strata, age-defined patient groups, haplotypes, and luciferase reporter activity.
resultsrs10118795 CT was associated with increased malaria susceptibility (OR = 1.584, 95% CI 1.068-2.350; p = 0.022), whereas rs55726619 CT showed a protective association (OR = 0.042, 95% CI 0.002-0.725; p < 0.001). rs55726619 showed the most consistent parasite-burden association, including with the highest parasite-density category. In children aged 1-5 years, rs10815393 CC was strongly enriched compared with patients aged ≥ 6 years (100.0% vs. 2.1%; χ
conclusionIL-33 variants, particularly rs55726619 and rs10815393, may influence P. falciparum susceptibility, parasite-burden response, and age-dependent host genetic effects, supporting IL-33/ST2 signaling as a relevant pathway for further validation.
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