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Autoimmune (type 1) diabetes

Delli, Ahmed LU and Lernmark, Åke LU (2013) In The Autoimmune Diseases p.575-585
Abstract
Autoimmune (type 1) diabetes (AI-DM) is a multistage disorder. Children are born genetically predisposed to putative environmental exposures. These trigger an aggressive, selective and chronic autoimmune response against the pancreatic islet beta cells. This stage is marked by autoantibodies against insulin, glutamic acid decarboxylase (GAD65), IA-2 and the ZnT8 transporter. Progression to clinical onset of diabetes is highly variable but the time to onset is shortened with an increased number of islet autoantibodies. Both islet autoantibodies and diabetes are associated with HLA-DQ on chromosome 6. More than 50 non-HLA genetic factors, mostly associated with the human immune response also contribute. It remains to be clarified to what... (More)
Autoimmune (type 1) diabetes (AI-DM) is a multistage disorder. Children are born genetically predisposed to putative environmental exposures. These trigger an aggressive, selective and chronic autoimmune response against the pancreatic islet beta cells. This stage is marked by autoantibodies against insulin, glutamic acid decarboxylase (GAD65), IA-2 and the ZnT8 transporter. Progression to clinical onset of diabetes is highly variable but the time to onset is shortened with an increased number of islet autoantibodies. Both islet autoantibodies and diabetes are associated with HLA-DQ on chromosome 6. More than 50 non-HLA genetic factors, mostly associated with the human immune response also contribute. It remains to be clarified to what extent HLA-DQ and the non-HLA genes contribute to the initiation of the chronic islet autoimmunity, progression to diabetes, or both. Insulin replacement therapy is still the only treatment as all attempts to halt the loss of beta cells by immunosuppression or immune modulation have failed so far. (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
Diabetes, type 1, Autoimmune diabetes, Islet autoimmunity, Islet autoantibodies, Insulitis.
in
The Autoimmune Diseases
editor
Rose, Noel; MacKay, Ian; and
pages
575 - 585
publisher
Academic Press
ISBN
0123849292
language
English
LU publication?
yes
id
f747aefb-a92a-459f-ab76-697893c09d3d (old id 3953435)
date added to LUP
2015-08-28 15:10:21
date last changed
2016-04-16 10:16:25
@inbook{f747aefb-a92a-459f-ab76-697893c09d3d,
  abstract     = {Autoimmune (type 1) diabetes (AI-DM) is a multistage disorder. Children are born genetically predisposed to putative environmental exposures. These trigger an aggressive, selective and chronic autoimmune response against the pancreatic islet beta cells. This stage is marked by autoantibodies against insulin, glutamic acid decarboxylase (GAD65), IA-2 and the ZnT8 transporter. Progression to clinical onset of diabetes is highly variable but the time to onset is shortened with an increased number of islet autoantibodies. Both islet autoantibodies and diabetes are associated with HLA-DQ on chromosome 6. More than 50 non-HLA genetic factors, mostly associated with the human immune response also contribute. It remains to be clarified to what extent HLA-DQ and the non-HLA genes contribute to the initiation of the chronic islet autoimmunity, progression to diabetes, or both. Insulin replacement therapy is still the only treatment as all attempts to halt the loss of beta cells by immunosuppression or immune modulation have failed so far.},
  author       = {Delli, Ahmed and Lernmark, Åke},
  editor       = {Rose, Noel and MacKay, Ian},
  isbn         = {0123849292},
  keyword      = {Diabetes,type 1,Autoimmune diabetes,Islet autoimmunity,Islet autoantibodies,Insulitis.},
  language     = {eng},
  pages        = {575--585},
  publisher    = {Academic Press},
  series       = {The Autoimmune Diseases},
  title        = {Autoimmune (type 1) diabetes},
  year         = {2013},
}