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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1937293
- author
- Larsson, Helena Elding
and Lernmark, Åke
LU
- organization
- publishing date
- 2011
- 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
- pmid:21481019
- 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
- 2016-04-04 09:22:04
- date last changed
- 2022-01-29 17:33:02
@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}},
doi = {{10.1111/j.1365-2796.2011.02386.x}},
volume = {{269}},
year = {{2011}},
}