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J Korean Med Assoc. 2009 Jul;52(7):677-687. Korean. Original Article. https://doi.org/10.5124/jkma.2009.52.7.677
Lee MS , Kim KA .
Department of Medicine, Sungkyunkwan University College of Medicine, Korea. mslee0923@skku.edu
Department of Medicine, Dongguk University College of Medicine, Korea. kyoung-ah.kim@duih.org
Abstract

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by selective autoimmune- mediated destruction of pancreatic islet beta- cells leading gradually to absolute insulin deficiency. T1D is under polygenic control. The HLA complex attributes 50% of the genetic risk for T1D while as many as 20 genes influence susceptibility to T1D. The autoimmune beta-cell destruction could be triggered by environmental factors. While the exact trigger of anti-islet autoimmunity remains elusive, it can lead to an imbalance between regulatory T cells and autoimmune effector T cells. During the initiation of insulitis, emerging evidences suggest that the infiltrating macrophages via toll-like receptor 2 (TLR2) activation lead to induction and amplification of insulitis. Following the priming of diabetogenic T-cells, autoreactive T effector cells destroy the beta cells by direct contact- dependent cytolysis or by soluble mediators secreted from macrophages or CD4 T effector cells. The hyperglycemia occurs late in its course after 80% of the beta cells have been destroyed. Although no current cure exists, refinement of genetic studies and islet autoantibodies has improved the ability to predict the risk of T1D and aid the establishment of rationally designed preventive therapies. Other strategies involve beta-cell replacement by islet transplantation. Extensive and long-term research on the efficacy of islet transplantation and preservation of beta-cell function is keenly needed.

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