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Vaccination against type 1 diabetes.

Larsson, Helena Elding and Lernmark, Åke LU (2011) In Journal of Internal Medicine 269. p.626-635
Abstract
The clinical onset of type 1 diabetes or autoimmune diabetes occurs after a prodrome of islet autoimmunity. The warning signals for the ensuing loss of pancreatic islet beta cells are autoantibodies against insulin, GAD65, IA-2, and ZnT8, alone or in combinations. Autoantibodies against e.g. insulin alone have only a minor risk for type 1 diabetes. However, progression to clinical onset is increased by the induction of multiple islet autoantibodies. At the time of clinical onset, insulitis may be manifest, which seem to reduce the efficacy of immunosuppression. Autoantigen-specific immunotherapy with alum-formulated GAD65 (Diamyd(®) ) show promise to reduce the loss of beta-cell function after the clinical onset of type 1 diabetes. The... (More)
The clinical onset of type 1 diabetes or autoimmune diabetes occurs after a prodrome of islet autoimmunity. The warning signals for the ensuing loss of pancreatic islet beta cells are autoantibodies against insulin, GAD65, IA-2, and ZnT8, alone or in combinations. Autoantibodies against e.g. insulin alone have only a minor risk for type 1 diabetes. However, progression to clinical onset is increased by the induction of multiple islet autoantibodies. At the time of clinical onset, insulitis may be manifest, which seem to reduce the efficacy of immunosuppression. Autoantigen-specific immunotherapy with alum-formulated GAD65 (Diamyd(®) ) show promise to reduce the loss of beta-cell function after the clinical onset of type 1 diabetes. The mechanisms are unclear but may involve the induction of T regulatory cells, which may suppress islet autoantigen reactivity. Past and on-going clinical trials have been safe. Future clinical trials, perhaps as combination autoantigen-specific immunotherapy may increase the efficacy to prevent the clinical onset in subjects with islet autoantibodies or preserve residual beta-cell function in newly diagnosed type 1 diabetes patients. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Internal Medicine
volume
269
pages
626 - 635
publisher
Wiley-Blackwell
external identifiers
  • wos:000290867900008
  • pmid:21481019
  • scopus:79956277614
ISSN
1365-2796
DOI
10.1111/j.1365-2796.2011.02386.x
language
English
LU publication?
yes
id
18bbf379-c1fd-403e-bdc6-8bfa953000a3 (old id 1937293)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21481019?dopt=Abstract
date added to LUP
2011-05-02 11:55:30
date last changed
2017-06-04 04:36:19
@article{18bbf379-c1fd-403e-bdc6-8bfa953000a3,
  abstract     = {The clinical onset of type 1 diabetes or autoimmune diabetes occurs after a prodrome of islet autoimmunity. The warning signals for the ensuing loss of pancreatic islet beta cells are autoantibodies against insulin, GAD65, IA-2, and ZnT8, alone or in combinations. Autoantibodies against e.g. insulin alone have only a minor risk for type 1 diabetes. However, progression to clinical onset is increased by the induction of multiple islet autoantibodies. At the time of clinical onset, insulitis may be manifest, which seem to reduce the efficacy of immunosuppression. Autoantigen-specific immunotherapy with alum-formulated GAD65 (Diamyd(®) ) show promise to reduce the loss of beta-cell function after the clinical onset of type 1 diabetes. The mechanisms are unclear but may involve the induction of T regulatory cells, which may suppress islet autoantigen reactivity. Past and on-going clinical trials have been safe. Future clinical trials, perhaps as combination autoantigen-specific immunotherapy may increase the efficacy to prevent the clinical onset in subjects with islet autoantibodies or preserve residual beta-cell function in newly diagnosed type 1 diabetes patients.},
  author       = {Larsson, Helena Elding and Lernmark, Åke},
  issn         = {1365-2796},
  language     = {eng},
  pages        = {626--635},
  publisher    = {Wiley-Blackwell},
  series       = {Journal of Internal Medicine},
  title        = {Vaccination against type 1 diabetes.},
  url          = {http://dx.doi.org/10.1111/j.1365-2796.2011.02386.x},
  volume       = {269},
  year         = {2011},
}