OBJECTIVEType 1 diabetes mellitus (T1DM) has been recognized as a T-cell mediated autoimmune disease, the migration of immune effector cells from the bloodstream into the pancreatic islet may be a crucial step in the pathogenesis of T1DM. However, a clinically applicable method for measuring pancreatic beta-cell specific T-cell function in cases of T1DM has not been established. Interferon-inducible protein-10 (IP-10) is a chemokine that promotes the migration of activated T cells. The aim of this study was to investigate the role of IP-10 in the pathogenesis of childhood T1DM.

METHODSSerum IP-10 levels were measured by ELISA in 50 children with T1DM and 30 healthy children, and the levels of autoantibodies [glutamic acid decarboxylase (GAD), isle tcell antibody (ICA), insulin autoantibody (IAA) and tyrosine phosphatase (IA-2)] in diabetic children were measured as well. Comparisons were made among groups divided by autoantibody condition and disease period.

RESULTSThe serum levels of IP-10 in patients with T1DM [(367 +/- 130) ng/L] were significantly higher than those in controls [(133 +/- 43) ng/L] (t = 9.49, P < 0.01). IP-10 levels in autoantibody positive [(385 +/- 147) ng/L] and negative diabetic children [(311 +/- 101) ng/L] were both higher than those in controls, but the difference was not significant. The serum levels of IP-10 among diabetic children who were positive for 1, 2 or 3 kinds of autoantibody did not show significant difference (F = 1.46, P > 0.05). IP-10 levels in newly diagnosed patients were much higher than those with disease period longer than 2 years (t = 4.30, P < 0.01), although both of them were higher than those in controls.

CONCLUSIONThe serum levels of IP-10 in children with T1DM were higher than those in controls, but they were not affected by either the presence of autoantibody or the number of positive autoantibodies. IP-10 levels decreased gradually with disease period prolonged.