ABSTRACT
Background: natural killer T [NKT] Cells are unique immunoregulatory cells reported to be deficient in many autoimmune disorders as systemic sclerosis with controversy as regards their role in IDDM. HLA-G is a non-classical HL4 class I molecule with immunotolerant function through T and NK cells inhibition but its role in IDDM is not defined. Bur aim was to evaluate NKT cells frequency and activity as well as the level and expression of HLA-G in children with IDDM to highlight their role in disease pathogenesis
Study design: this study included 28 children with IDDM who attended Mansoura University Children's Hospital consecutively from June, 2003 to March, 2004. A group of 18 healthy children with matched age and sex having no family history of diabetes mellitus served as control. All subjects were exposed to thorough history and clinical examination beside routine investigations that included random blood sugar and glycosylated hemoglobin. NKT cell receptors [Valfa24-JalfaQ] were assessed by ELISA before and after mitogen stimulation. NKT cell receptor expression was also assessed by quantitative reverse transcriptase polymerase chain reaction [RT-PCR]. Soluble HLA-G was also determined by ELISA and its expression was assessed by RT-PCR
Results: NKT cell receptors were significantly lower in patients before and after mitogen stimulation compared to control [p<0.001]. Similarly, NKT cell receptor expression was significantly lower in patients than control [P<0.001]. On the other hand, sHLA-G and HLA-G expression were significantly higher in patients than control [p<0.001] A. highly significant negative correlation was found be between NKT receptors and HLA-G [p<0.001]. But no significant correlation was observed between NKT cell receptors or HLA-G and either age, duration of illness, random blood sugar, dose of insulin or level of glycosylated hemoglobin
Conclusion: NXT cells frequency and activity are decreased in children with IDDM which may contribute to disease development. HLA-G level and expression are increased in diabetic children suggesting a role for this molecule in DDM pathogenesis