Immunomodulation with human recombinant autoantigens
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/212444
- author
- Lernmark, A and Agardh, Carl-David LU
- organization
- publishing date
- 2005
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Unit on Vascular Diabetic Complications (013241510)
- id
- ec1e8edd-017c-4372-bf65-2d125680932d (old id 212444)
- date added to LUP
- 2016-04-01 11:50:26
- date last changed
- 2022-01-26 19:03:29
@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}},
doi = {{10.1016/j.it.2005.08.015}},
volume = {{26}},
year = {{2005}},
}