|
KMID : 1134220090290020168
|
|
Hanyang Medical Reviews
2009 Volume.29 No. 2 p.168 ~ p.175
|
|
|
Pathogenesis of Type 1 Diabetes
|
|
Kim Kyoung-Ah
Lee Myung -Shik
|
|
|
Abstract
|
|
|
Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease characterized by selective destruction of pancreatic islet β-cells causing insulin deficiency. T1D has been shown to be a polygenic trait, associated with several loci, among
which the human leukocyte antigen (HLA) region accounts for 40% of the genetic risk to develop T1D. The β-cell autoimmune response is triggered by environmental or unknown events in the predisposing genetic background. The triggers of autoimmunity can lead to a localized imbalance between regulatory T cells and autoimmune effector
T cells. The macrophages and autoreactive lymphocytes infiltrate the islets and the interaction of β-cells and immune cells leads to inductionamplification of insulitis and loss of β-cells. T cells destroy β-cells in a direct cytotoxic manner or
influence the induction of β-cell apoptosis through the release of cytotoxic molecules, such as cytokines. The autoimmune process progresses subclinically for many years in the majority of patients, and clinical symptom do not appear until more than 80% of β-cells have been destroyed. Although no current “cure” exists, there is a major effort to develop immunotherapies to prevent or halt the disorder that still requires much research to fully understand exact triggering events leading to autoimmune activation. Other strategies involve β- cell replacement by islet transplantation, but researchs to enhance the islet mass transplanted and preserve β-cell function are necessary.
|
|
|
KEYWORD
|
|
|
Pancreatic β-cell, Type 1 diabetes mellitus, Autoimmunity, Apoptosis, Preventive trial
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|