Cytokine · 2026
Interleukin gene polymorphisms (IL-6, IL-10, IL-17 a, IL-18) predict beta-thalassemia major susceptibility and inflammatory profiles in Iraqi children: A genetic risk score analysis.
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Hoidy Wisam Hindawi, Chyad Doaa Hadi, Essa Ali Mohsen, Essa Shaimaa Mohsen, Al-Saadi Mohammed Hamza
Аннотация
BACKGROUND: This research aims to evaluate the correlation between the four interleukin gene polymorphisms, namely (IL-6 -174 G/C, IL-10 -1082 A/G, IL-17 A -197 G/A, IL-18 -137 G/C), and the predisposition to develop beta-thalassemia major in Iraqi children, in addition to analyzing how these polymorphisms impact the serum cytokine levels.
METHODS: This case-control study was conducted at the Thalassemia Center, Baghdad Teaching Hospital, Iraq, in 2024, and included 311 children suffering from beta-thalassemia major and 390 healthy controls, matched by age and sex. Genotyping was conducted using the T-ARMS. Serum levels of IL-6, IL-10, IL-17 A, and IL-18 were determined using enzyme-linked immunosorbent assay (ELISA). Statistical methods such as logistic regression, Hardy Weinberg equilibrium, haplotype, and genetic risk score were utilized.
RESULTS: All four polymorphisms were significantly associated with disease susceptibility. The increasing risk demonstrated was due to the polymorphisms such as the IL-6 174C allele (OR = 1.61, 95% CI: 1.31-1.98, p < 0.001), IL-10 -1082 G allele (OR = 1.78, 95% CI: 1.45-2.19, p < 0.001), IL-17 A -197 A allele (OR = 2.06, 95% CI: 1.67-2.53, p < 0.001), and IL-18 137C allele (OR = 1.90, 95% CI: 1.54-2.34, p < 0.001). The test showed very strong correlations between genotypes, and phenotypes, with the associated risk allele proxies having higher levels of the pro- inflammatory cytokines and lower levels of IL-10. Children carrying 7-8 risk alleles had a 12.35-fold higher risk of disease (95% CI: 7.18-21.25, p < 0.001).
CONCLUSIONS: In Iraqi children, the polymorphisms found within the interleukins were associated with inflammatory profiles and susceptibility to beta thalassemia major. These genetic variants may influence inflammatory pathways that contribute to disease complexity. Due to the case-control design, these findings demonstrate associations rather than causal relationships between interleukin polymorphisms and beta-thalassemia susceptibility.
METHODS: This case-control study was conducted at the Thalassemia Center, Baghdad Teaching Hospital, Iraq, in 2024, and included 311 children suffering from beta-thalassemia major and 390 healthy controls, matched by age and sex. Genotyping was conducted using the T-ARMS. Serum levels of IL-6, IL-10, IL-17 A, and IL-18 were determined using enzyme-linked immunosorbent assay (ELISA). Statistical methods such as logistic regression, Hardy Weinberg equilibrium, haplotype, and genetic risk score were utilized.
RESULTS: All four polymorphisms were significantly associated with disease susceptibility. The increasing risk demonstrated was due to the polymorphisms such as the IL-6 174C allele (OR = 1.61, 95% CI: 1.31-1.98, p < 0.001), IL-10 -1082 G allele (OR = 1.78, 95% CI: 1.45-2.19, p < 0.001), IL-17 A -197 A allele (OR = 2.06, 95% CI: 1.67-2.53, p < 0.001), and IL-18 137C allele (OR = 1.90, 95% CI: 1.54-2.34, p < 0.001). The test showed very strong correlations between genotypes, and phenotypes, with the associated risk allele proxies having higher levels of the pro- inflammatory cytokines and lower levels of IL-10. Children carrying 7-8 risk alleles had a 12.35-fold higher risk of disease (95% CI: 7.18-21.25, p < 0.001).
CONCLUSIONS: In Iraqi children, the polymorphisms found within the interleukins were associated with inflammatory profiles and susceptibility to beta thalassemia major. These genetic variants may influence inflammatory pathways that contribute to disease complexity. Due to the case-control design, these findings demonstrate associations rather than causal relationships between interleukin polymorphisms and beta-thalassemia susceptibility.