Autoantibodies and cytokines levels in type 1 diabetic patients

ABSTRACT

Type 1 diabetes is characterized by a complete or near-complete insulin deficiency caused by an immune-mediated selective destruction of the insulin-producing beta-cells in the Islets of Langerhans. Inflammatory mechanisms play a key role in the pathogenesis of type 1 diabetes. Many findings suggest that the Islet autoantibody status in type 1 diabetes is linked to disease activity. To investigate the hypothesis that the systemic immunoregulatory balance, as defined by levels of circulating cytokines, is associated with Islet autoantibody status. Cytokines [IL-2, IL-4, IL-5, IL-10, TNF-beta and INF-gamma] and Islet autoantibodies [ICA, GADA, IA-2] were measured in 56 patients with insulin dependent diabetes mellitus [IDDM] and 20 healthy control patients. The three proinflammatory cytokines measured [interleukin-2 [IL-2], interferon gamma [IFN-gamma] and tumor necrosis factor-beta [TNF-beta]], both TNF-beta [50.0 +/- 5.9] [63.4 +/- 5.4] and INF-gamma [13.8 +/- 10.9] [13.7 +/- 5.5] showed a significant increase [P <0.05] with Islet autoantibody positivity, while the other three cytokines, [IL-4, IL-5 and IL-10], only IL-4 showed a positive increase [54.4 +/- 1.4] with Islet autoantibody positivity although it is non- significant association. The study reveals the possibility of the of Islet autoantibodies in the domination of proinflammatory cytokines over the immunoregulatory cytokines