Abstract
The pathophysiologic mechanisms in type 1 diabetes (T1DM) involve loss of islet β-cell secretory function caused by selective killing of these
cells primarily by aggressive autoimmune responses involving both cellular and humoral immune pathways. Inflammatory cells heavily infiltrate pancreatic islets leading to insulitis where CD8+ T lymphocytes are thought to be responsible for selective and specific killing of β-cells.
The complex etiology of T1DM involves a strong genetic predisposition, mainly human leukocyte antigen class II genes, and several putative
environmental factors, which are thought to trigger autoimmunity or progression to clinical T1DM.
A preclinical prodrome in T1DM may vary in duration in which one or more islet autoantibodies may precede insulitis and predict the disease
at the early stages of pathologic insult. In genetically susceptible individuals with islet autoantibodies, metabolic indicators such as insulin release abnormalities and insulin resistance may best predict T1DM especially near clinical onset.
Based on the improving understanding of the etiopathogenesis of T1DM, several clinical trials have been launched aiming at halting the
autoimmunity responses, retarding disease progression or preserving remaining β-cell function after clinical onset.
cells primarily by aggressive autoimmune responses involving both cellular and humoral immune pathways. Inflammatory cells heavily infiltrate pancreatic islets leading to insulitis where CD8+ T lymphocytes are thought to be responsible for selective and specific killing of β-cells.
The complex etiology of T1DM involves a strong genetic predisposition, mainly human leukocyte antigen class II genes, and several putative
environmental factors, which are thought to trigger autoimmunity or progression to clinical T1DM.
A preclinical prodrome in T1DM may vary in duration in which one or more islet autoantibodies may precede insulitis and predict the disease
at the early stages of pathologic insult. In genetically susceptible individuals with islet autoantibodies, metabolic indicators such as insulin release abnormalities and insulin resistance may best predict T1DM especially near clinical onset.
Based on the improving understanding of the etiopathogenesis of T1DM, several clinical trials have been launched aiming at halting the
autoimmunity responses, retarding disease progression or preserving remaining β-cell function after clinical onset.
| Original language | English |
|---|---|
| Title of host publication | Textbook of Diabetes |
| Editors | Richard I. G. Holt, Clive S. Cockram, Allan Flyvbjerg, Barry J. Goldstein |
| Publisher | Wiley-Blackwell |
| Pages | 141-152 |
| ISBN (Print) | 9781405191814 |
| DOIs | |
| Publication status | Published - 2010 |
Subject classification (UKÄ)
- Clinical Medicine
Free keywords
- Type 1 diabetes
- autoimmune diabetes
- insulin-dependent diabetes
- Islet autoimmunity
- Islet autoantibodies
- HLA genes
- pathogenesis.
