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Immunomodulation with human recombinant autoantigens

Lernmark, A and Agardh, Carl-David LU (2005) In Trends in Immunology 26(11). p.608-612
Abstract
The loss of beta cells in type 1 diabetes is the consequence of a T cell-dependent autoimmune attack. Autoantibodies against GAD65 (Mr 65.000 isoform of glutamic acid decarboxylase), IA-2 (insulinoma-associated protein IA-2) or insulin, alone or in combination, predict disease. Preclinical studies in spontaneously diabetic rodents suggest that immunomodulation with autoantigens might alter the course of autoimmune diabetes. Oral insulin reduces the development of diabetes in risk subjects with high insulin autoantibody levels. Giving alum-formulated GAD65 to patients classified with latent autoimmune diabetes of the adult (LADA) is safe and suggests possible immunomodulating effects of GAD65. Future immunomodulation trials might better... (More)
The loss of beta cells in type 1 diabetes is the consequence of a T cell-dependent autoimmune attack. Autoantibodies against GAD65 (Mr 65.000 isoform of glutamic acid decarboxylase), IA-2 (insulinoma-associated protein IA-2) or insulin, alone or in combination, predict disease. Preclinical studies in spontaneously diabetic rodents suggest that immunomodulation with autoantigens might alter the course of autoimmune diabetes. Oral insulin reduces the development of diabetes in risk subjects with high insulin autoantibody levels. Giving alum-formulated GAD65 to patients classified with latent autoimmune diabetes of the adult (LADA) is safe and suggests possible immunomodulating effects of GAD65. Future immunomodulation trials might better ascertain subjects based on HLA genetic risk factors, the level of insulin that is still produced or by combining autoantigens with, for example, anti-CD3 antibodies, to induce antigen-specific tolerance and thereby a long-lasting protection for beta cells. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Trends in Immunology
volume
26
issue
11
pages
608 - 612
publisher
Elsevier
external identifiers
  • wos:000233375900010
  • pmid:16153889
  • scopus:28444486947
ISSN
1471-4981
DOI
10.1016/j.it.2005.08.015
language
English
LU publication?
yes
id
ec1e8edd-017c-4372-bf65-2d125680932d (old id 212444)
date added to LUP
2007-08-15 12:39:26
date last changed
2017-01-01 04:35:34
@article{ec1e8edd-017c-4372-bf65-2d125680932d,
  abstract     = {The loss of beta cells in type 1 diabetes is the consequence of a T cell-dependent autoimmune attack. Autoantibodies against GAD65 (Mr 65.000 isoform of glutamic acid decarboxylase), IA-2 (insulinoma-associated protein IA-2) or insulin, alone or in combination, predict disease. Preclinical studies in spontaneously diabetic rodents suggest that immunomodulation with autoantigens might alter the course of autoimmune diabetes. Oral insulin reduces the development of diabetes in risk subjects with high insulin autoantibody levels. Giving alum-formulated GAD65 to patients classified with latent autoimmune diabetes of the adult (LADA) is safe and suggests possible immunomodulating effects of GAD65. Future immunomodulation trials might better ascertain subjects based on HLA genetic risk factors, the level of insulin that is still produced or by combining autoantigens with, for example, anti-CD3 antibodies, to induce antigen-specific tolerance and thereby a long-lasting protection for beta cells.},
  author       = {Lernmark, A and Agardh, Carl-David},
  issn         = {1471-4981},
  language     = {eng},
  number       = {11},
  pages        = {608--612},
  publisher    = {Elsevier},
  series       = {Trends in Immunology},
  title        = {Immunomodulation with human recombinant autoantigens},
  url          = {http://dx.doi.org/10.1016/j.it.2005.08.015},
  volume       = {26},
  year         = {2005},
}