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Autoantibodies in diabetes.

Pihoker, C; Gilliam, L K; Hampe, C S and Lernmark, Åke LU (2005) In Diabetes 54(Dec). p.52-61
Abstract
Islet cell autoantibodies are strongly associated with the development of type 1 diabetes. The appearance of autoantibodies to one or several of the autoantigens—GAD65, IA-2, or insulin—signals an autoimmune pathogenesis of ß-cell killing. A ß-cell attack may be best reflected by the emergence of autoantibodies dependent on the genotype risk factors, isotype, and subtype of the autoantibodies as well as their epitope specificity. It is speculated that progression to ß-cell loss and clinical onset of type 1 diabetes is reflected in a developing pattern of epitope-specific autoantibodies. Although the appearance of autoantibodies does not follow a distinct pattern, the presence of multiple autoantibodies has the highest positive predictive... (More)
Islet cell autoantibodies are strongly associated with the development of type 1 diabetes. The appearance of autoantibodies to one or several of the autoantigens—GAD65, IA-2, or insulin—signals an autoimmune pathogenesis of ß-cell killing. A ß-cell attack may be best reflected by the emergence of autoantibodies dependent on the genotype risk factors, isotype, and subtype of the autoantibodies as well as their epitope specificity. It is speculated that progression to ß-cell loss and clinical onset of type 1 diabetes is reflected in a developing pattern of epitope-specific autoantibodies. Although the appearance of autoantibodies does not follow a distinct pattern, the presence of multiple autoantibodies has the highest positive predictive value for type 1 diabetes. In the absence of reliable T-cell tests, dissection of autoantibody responses in subjects of genetic risk should prove useful in identifying triggers of islet autoimmunity by examining seroconversion and maturation of the autoantibody response that may mark time to onset of type 1 diabetes. The complexity of the disease process is exemplified by multiple clinical phenotypes, including autoimmune diabetes masquerading as type 2 diabetes in youth and adults. Autoantibodies may also provide prognostic information in clinically heterogeneous patient populations when examined longitudinally. (Less)
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author
publishing date
type
Contribution to journal
publication status
published
subject
in
Diabetes
volume
54
issue
Dec
pages
52 - 61
publisher
American Diabetes Association Inc.
ISSN
1939-327X
language
English
LU publication?
no
id
02e34b0a-d443-4850-bfc7-4dd673c30cc9 (old id 1133063)
alternative location
http://diabetes.diabetesjournals.org/cgi/content/full/54/suppl_2/S52
date added to LUP
2008-06-25 14:30:29
date last changed
2016-06-29 09:08:36
@article{02e34b0a-d443-4850-bfc7-4dd673c30cc9,
  abstract     = {Islet cell autoantibodies are strongly associated with the development of type 1 diabetes. The appearance of autoantibodies to one or several of the autoantigens—GAD65, IA-2, or insulin—signals an autoimmune pathogenesis of ß-cell killing. A ß-cell attack may be best reflected by the emergence of autoantibodies dependent on the genotype risk factors, isotype, and subtype of the autoantibodies as well as their epitope specificity. It is speculated that progression to ß-cell loss and clinical onset of type 1 diabetes is reflected in a developing pattern of epitope-specific autoantibodies. Although the appearance of autoantibodies does not follow a distinct pattern, the presence of multiple autoantibodies has the highest positive predictive value for type 1 diabetes. In the absence of reliable T-cell tests, dissection of autoantibody responses in subjects of genetic risk should prove useful in identifying triggers of islet autoimmunity by examining seroconversion and maturation of the autoantibody response that may mark time to onset of type 1 diabetes. The complexity of the disease process is exemplified by multiple clinical phenotypes, including autoimmune diabetes masquerading as type 2 diabetes in youth and adults. Autoantibodies may also provide prognostic information in clinically heterogeneous patient populations when examined longitudinally.},
  author       = {Pihoker, C and Gilliam, L K and Hampe, C S and Lernmark, Åke},
  issn         = {1939-327X},
  language     = {eng},
  number       = {Dec},
  pages        = {52--61},
  publisher    = {American Diabetes Association Inc.},
  series       = {Diabetes},
  title        = {Autoantibodies in diabetes.},
  volume       = {54},
  year         = {2005},
}