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SNPs at the IL-2, IL-12, TNF-α and TGF-β1 regulatory gene regions are probably important for Toxoplasma gondii congenital transmission and disease severity in humans
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DOI：10.1016/j.micinf.2025.105565.png)
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Abstract
En 中文
Toxoplasma gondii infection in pregnant females can cause congenital toxoplasmosis. Although maternal and infant immune profiles appear to play a role, studies on this topic are scarce. We analyzed SNPs in the regulatory regions of cytokine genes in 30 mother-newborn pairs, five mothers and two infants with known status, with respect to vertical transmission and the clinical outcome of those infected. Polymorphisms in the IL-2, IL-10, IL-12, IL-17, TNF-α, and TGF-β1 gene promoter or regulatory regions were obtained by sequencing, and genotype and allele frequencies were related to transmission and clinical outcome of the offspring. In children, the polymorphic "G" TNF-α -308 allele, as well as the related low- and high-level homozygous GG or TT genotypes of the 3'UTR region of the IL-12reg gene, were associated with congenital infection. Both cytokines have been shown to be expressed in the cyto- and syncytiotrophoblast; therefore, the fetus might be able to regulate infection at the placental level. In mothers of infected children, the T allele of the IL-12reg 3'UTR gene was associated with more severe disease in their offspring, suggesting that a strong maternal response reduces parasite spread in the fetus. Furthermore, SNPs in the promoter region of IL2 and TGF-β1 were associated with elevated levels and milder disease in children with congenital infection, which is congruent with a regulation of a strong, damaging, inflammatory response. Our results suggest that some up and down regulatory cytokine genes may predispose to vertical transmission or disease severity in congenital toxoplasmosis.
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