Autoimmune type 1 diabetes.
Delli, Ahmed LU ; Larsson, Helena LU ; Ivarsson, Sten LU and Lernmark, Åke LU
(2010)
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:
https://lup.lub.lu.se/record/3953436
- author
- Delli, Ahmed
LU
; Larsson, Helena
LU
; Ivarsson, Sten
LU
and Lernmark, Åke
LU
- organization
- publishing date
- 2010
- 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.
- host publication
- 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
- 2016-04-04 11:32:03
- date last changed
- 2018-11-21 21:05:28
@inbook{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}},
booktitle = {{Textbook of Diabetes}},
editor = {{Holt, Richard I. G. and Cockram, Clive S. and Flyvbjerg, Allan and Goldstein, Barry J.}},
isbn = {{9781405191814}},
keywords = {{Type 1 diabetes; autoimmune diabetes; insulin-dependent diabetes; Islet autoimmunity; Islet autoantibodies; HLA genes; pathogenesis.}},
language = {{eng}},
pages = {{141--152}},
publisher = {{Wiley-Blackwell}},
title = {{Autoimmune type 1 diabetes.}},
url = {{http://dx.doi.org/10.1002/9781444324808}},
doi = {{10.1002/9781444324808}},
year = {{2010}},
}