RESUMO
Type I diabetes is an autoimmune disease that results from destruction of pancreatic islet beta cells by autoreactive cells and their mediators. The prominent feature is a dysregulated humoral and cellular immunity with altered production of and response to T cell-derived cytokines and a shift in T-helper [Th] cell differentiation. Islet cells inflammation in autoimmune diabetes starts from benign peri-insulitis with dominance of Th2 cells to destructive intra-insulitis with dominance of Th1 cells. The aim of this study was to evaluate the role of IL-10 and IL-18 as representatives, of Th2 and Th1 cell activities in the ; pathogenesis of type I diabetes mellitus. The study was conducted on 30 children [mean age 9.30 +/- 2.19 years] with newly diagnosed type-I diabetes [within 3 months of onset of symptoms] and on 15 healthy age and sex matched children as a control group. Determination of IL-10 and IL-18 levels in peripheral blood mononuclear cells [PBMCs] culture supernatant of aN patients and controls were done before and after stimulation with phytohemagglutinin [PHA]. Statistical analysis of the result showed that: [1]- The mean level of IL-10 was significantly lower in diabetic children than in controls before stimulation [t=3.168; P<0,01]. After stimulation with PHA, the mean IL-10 level was significantly higher in diabetic children than in controls [t=3.509; P<0.01], this was due to a significant rise of IL-10 level in diabetic children [t=3.740, P<0.01], and a significant reduction of IL-10 level in control children after stimulation with PHA [t=4.958; P<0.01]. [2]- Mean IL-18 levels in diabetic children were significantly higher than those of controls both before [t=2.056; P<0.05] and after stimulation with PHA [t=2.099; P<0.05]. Stimulation with PHA was associated with a significant rise in IL- 18 levels both in patients [t=2.073; P<0.050 and controls [t=2.480; P<0.05]
Conclusion: children with recently diagnosed type-I diabetes have an abnormal cellular immunity with Th1 cytokine dominance, an important factor for pancreatic islet cell destruction. These abnormalities might be more pronounced if studied earlier before clinical disease onset. Further studies are needed to know whether the development of type I diabetes could be prevented by correcting the Th2/Th1 cytokine shift