Pathogenesis of Type 1 Diabetes.
- Author:
Kyoung Ah KIM
1
;
Myung Shik LEE
Author Information
1. Department of Medicine, Dongguk University Ilsan Hospital, Dongguk University School of Medicine, Goyang, Korea.
- Publication Type:Original Article
- Keywords:
Pancreatic beta-cell;
Type 1 diabetes mellitus;
Autoimmunity;
Apoptosis;
Preventive trial
- MeSH:
Apoptosis;
Autoimmune Diseases;
Autoimmunity;
Cytokines;
Diabetes Mellitus, Type 1;
Humans;
Immunotherapy;
Insulin;
Islets of Langerhans;
Islets of Langerhans Transplantation;
Leukocytes;
Lymphocytes;
Macrophages;
Multifactorial Inheritance;
T-Lymphocytes;
T-Lymphocytes, Regulatory;
Transplants
- From:Hanyang Medical Reviews
2009;29(2):168-175
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease characterized by selective destruction of pancreatic islet betacells 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 betacell 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 betacells and immune cells leads to inductionamplification of insulitis and loss of betacells. T cells destroy betacells in a direct cytotoxic manner or influence the induction of betacell 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 betacells 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 toautoimmune activation. Other strategies involve beta- cell replacement by islet transplantation, but researchs to enhance the islet mass transplanted and preserve beta-cell function are necessary.
