Serum IL-1, IL-2, TNFα and INFγ Levels of Patients with Type 1 Diabetes Mellitus and their Siblings

• DOI: 10.1515/jpem.2003.16.2.203
• Publication Date: 2011-04-15T11:08:03Z
• Authors: G. Özer; Ζ. Teker; S. Çetiner; M. Yılmaz; A.K. Topaloglu; N. Önenli-Mungan; B. Yüksel
• Keywords: Male; 0301 basic medicine; Adolescent; TNF?; Type 1 diabetes mellitus; Body Mass Index; Diabetic Ketoacidosis; Interferon-gamma; 03 medical and health sciences; INF?; Humans; Child; Glycated Hemoglobin; 0303 health sciences; Tumor Necrosis Factor-alpha; IL-2; Siblings; Body Weight; Infant; Lipids; Body Height; 3. Good health; Diabetes Mellitus, Type 1; Child, Preschool; Cytokines; Interleukin-2; IL-1?; Female; Interleukin-1

Type 1 diabetes mellitus (DM) develops as a result of autoimmune destruction of the pancreatic beta-cells. The aim of this study was to explore possible associations between serum levels of cytokines, IL-1, IL-2, TNFalpha and INFgamma and metabolic parameters in children with type 1 DM and their non-diabetic siblings to determine whether these cytokines could be indicators of disordered immune regulation. The study population consisted of 41 children with type 1 DM, 32 non-diabetic siblings, and 28 healthy controls. Children with DM were divided into three subgroups: 1) newly diagnosed patients with diabetic ketoacidosis (ND + DKA), 2) newly diagnosed patients without DKA (ND - DKA), and 3) previously diagnosed patients (PD). The highest serum IL-1alpha level was found in the ND - DKA group, which was significant compared to both the ND + DKA (p < 0.05) and the siblings (S) (p < 0.005). IL-2 levels were similar among all groups. The highest TNFalpha level was observed in the ND + DKA group, which was significant against the ND - DKA (p < 0.05), PD (p < 0.001), S (p < 0.05), and control (C) (p < 0.005) groups. TNFalpha concentration in the PD group was significantly lower than those of S (p< 0.005) and C (p < 0.001) groups. The ND - DKA group had the highest INFgamma and this was statistically significant when compared with the S (p < 0.005) and C (p < 0.05) groups. Both the newly diabetics and all diabetics as a group had statistically significantly higher INFgamma levels than both the S (p < 0.01 for both) and C (p < 0.05 for both) groups. In the diabetics as a whole group, TNFalpha showed correlations with INFgamma (r = 0.370, p < 0.05). IL-1 showed correlation with TNFalpha (r = 0.368, p < 0.05) INFgamma (r = 0.796, p < 0.001) and IL-2 (r = 0.862, p < 0.001) in the all diabetics group. IL-2 was correlated with TNFalpha (r = 0.320, p < 0.05) and INFgamma (r = 0.754, p < 0.01) in the all diabetics group. In conclusion, our results suggest that proinflammatory cytokines TNFalpha, INFgamma, IL-1alpha and IL-2 may play important roles alone or in combination in the pathogenesis of type 1 diabetes mellitus.