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Autoimmune type 1 diabetes.

Delli, Ahmed LU ; Larsson, Helena LU ; Ivarsson, Sten LU and Lernmark, Åke LU (2010) In Textbook of Diabetes p.141-152
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... (More)
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. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
Type 1 diabetes, autoimmune diabetes, insulin-dependent diabetes, Islet autoimmunity, Islet autoantibodies, HLA genes, pathogenesis.
in
Textbook of Diabetes
editor
Holt, Richard I. G.; Cockram, Clive S.; Flyvbjerg, Allan and Goldstein, Barry J.
pages
141 - 152
publisher
Wiley-Blackwell
ISBN
9781405191814
DOI
10.1002/9781444324808
language
English
LU publication?
yes
id
efed834d-6f9e-4d05-84d4-9e481ce65876 (old id 3953436)
date added to LUP
2013-10-24 17:08:54
date last changed
2016-04-16 09:21:45
@misc{efed834d-6f9e-4d05-84d4-9e481ce65876,
  abstract     = {The pathophysiologic mechanisms in type 1 diabetes (T1DM) involve loss of islet β-cell secretory function caused by selective killing of these <br/><br>
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. <br/><br>
The complex etiology of T1DM involves a strong genetic predisposition, mainly human leukocyte antigen class II genes, and several putative <br/><br>
environmental factors, which are thought to trigger autoimmunity or progression to clinical T1DM. <br/><br>
A preclinical prodrome in T1DM may vary in duration in which one or more islet autoantibodies may precede insulitis and predict the disease <br/><br>
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. <br/><br>
Based on the improving understanding of the etiopathogenesis of T1DM, several clinical trials have been launched aiming at halting the <br/><br>
autoimmunity responses, retarding disease progression or preserving remaining β-cell function after clinical onset.},
  author       = {Delli, Ahmed and Larsson, Helena and Ivarsson, Sten and Lernmark, Åke},
  editor       = {Holt, Richard I. G. and Cockram, Clive S. and Flyvbjerg, Allan and Goldstein, Barry J.},
  isbn         = {9781405191814},
  keyword      = {Type 1 diabetes,autoimmune diabetes,insulin-dependent diabetes,Islet autoimmunity,Islet autoantibodies,HLA genes,pathogenesis.},
  language     = {eng},
  pages        = {141--152},
  publisher    = {ARRAY(0xac43490)},
  series       = {Textbook of Diabetes},
  title        = {Autoimmune type 1 diabetes.},
  url          = {http://dx.doi.org/10.1002/9781444324808},
  year         = {2010},
}