Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase

Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in β cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive toleranc...

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Autores principales: Jaeckel, Elmar, Klein, Ludger, Martin-Orozco, Natalia, von Boehmer, Harald
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2003
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193961/
https://www.ncbi.nlm.nih.gov/pubmed/12796471
http://dx.doi.org/10.1084/jem.20030215
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author Jaeckel, Elmar
Klein, Ludger
Martin-Orozco, Natalia
von Boehmer, Harald
author_facet Jaeckel, Elmar
Klein, Ludger
Martin-Orozco, Natalia
von Boehmer, Harald
author_sort Jaeckel, Elmar
collection PubMed
description Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in β cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes.
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spelling pubmed-21939612008-04-11 Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase Jaeckel, Elmar Klein, Ludger Martin-Orozco, Natalia von Boehmer, Harald J Exp Med Article Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in β cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes. The Rockefeller University Press 2003-06-16 /pmc/articles/PMC2193961/ /pubmed/12796471 http://dx.doi.org/10.1084/jem.20030215 Text en Copyright © 2003, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Jaeckel, Elmar
Klein, Ludger
Martin-Orozco, Natalia
von Boehmer, Harald
Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
title Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
title_full Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
title_fullStr Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
title_full_unstemmed Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
title_short Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase
title_sort normal incidence of diabetes in nod mice tolerant to glutamic acid decarboxylase
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193961/
https://www.ncbi.nlm.nih.gov/pubmed/12796471
http://dx.doi.org/10.1084/jem.20030215
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