Dysregulated IL-6, IL-10, and IL-17 expression in Iraqi children with type 1 diabetes: correlation with clinical parameters and diagnostic potential.

Abstract

Diabetes triggering autoimmune mechanisms in populations with specific environmental contacts remain partially explored. This study aimed to determine expression levels of three interleukins (IL-6, IL-10, IL-17) in T1DM Iraqi children and their associations with clinical parameters. A case-control study compared 188 T1DM patients with 250 healthy children. Quantitative real-time PCR assessed gene expression of IL-6, IL-10, and IL-17 in peripheral blood mononuclear cells (PBMCs). ELISA assays quantified serum cytokines. Genetic haplotype mapping was performed in silico for polymorphisms of selected interleukin genes. T1DM patients showed strong expression of pro-inflammatory IL-6 (fold change 3.42, p < 0.001) and IL-17 (fold change 2.87, p < 0.001) with diminished anti-inflammatory IL-10 expression (fold change 0.38, p < 0.001). Associations were noted with HbA1c, disease duration, and age at diagnosis. Increased T1DM susceptibility was linked with haplotypes GCAA-IL-6, ATA-IL-10, AGT-IL-17. Combined interleukin expression score showed good diagnostic sensitivity (AUC = 0.924). Iraqi children with T1DM exhibited a pro-inflammatory cytokine profile creating immunological imbalance. This contributes to T1DM immunopathology understanding in this population and could aid in developing population-specific diagnostic and treatment approaches. Iraqi children with T1DM exhibit dysregulated cytokine expression with elevated pro-inflammatory IL-6 and IL-17, and suppressed anti-inflammatory IL-10. Population-specific genetic haplotypes (GCAA-IL-6, ATA-IL-10, AGT-IL-17) increase T1DM susceptibility in Iraqi children. First comprehensive study characterizing interleukin gene expression profiles in Iraqi pediatric T1DM population. Enables development of population-specific diagnostic biomarkers for T1DM in resource-limited settings.