Glutamic acid decarboxylase - Gene to antigen to disease
Lernmark, Å LU
(1996)
In Journal of Internal Medicine
240(5).
p.259-277
- Abstract
Glutamic acid decarboxylase (GAD) enzymes catalyse the formation of gamma-aminobuturic acid (GABA), which is a major transmittor in the central nervous system but also exerts functions in peripheral organs. Recent molecular analyses have revealed surprising new roles for the GAD isoforms in human diseases of autoimmune character including neurological disorders and insulin-dependent diabetes. In the 1995 Frontiers in Medicine Symposium, the coauthors of this review discussed the genetics, cell biology, molecular immunology and the role of GAD as autoantigens in human autoimmunity. Studies on disease diagnosis, prediction, and prognosis have revealed unique patterns of reactivities in both cellular and humoral immune responses. Further... (More)
Glutamic acid decarboxylase (GAD) enzymes catalyse the formation of gamma-aminobuturic acid (GABA), which is a major transmittor in the central nervous system but also exerts functions in peripheral organs. Recent molecular analyses have revealed surprising new roles for the GAD isoforms in human diseases of autoimmune character including neurological disorders and insulin-dependent diabetes. In the 1995 Frontiers in Medicine Symposium, the coauthors of this review discussed the genetics, cell biology, molecular immunology and the role of GAD as autoantigens in human autoimmunity. Studies on disease diagnosis, prediction, and prognosis have revealed unique patterns of reactivities in both cellular and humoral immune responses. Further work will be needed to establish whether the GAD molecules can be used to treat autoimmune diseases.
(Less)
- author
- Lernmark, Å
LU
- publishing date
- 1996-01-01
- type
- Contribution to journal
- publication status
- published
- in
- Journal of Internal Medicine
- volume
- 240
- issue
- 5
- pages
- 259 - 277
- publisher
- Wiley-Blackwell
- external identifiers
-
- scopus:0029683483
- pmid:8946809
- ISSN
- 0954-6820
- DOI
- 10.1046/j.1365-2796.1996.27859000.x
- language
- English
- LU publication?
- no
- id
- 02c2efd4-7af1-4980-a68e-325c605cd41d
- date added to LUP
- 2019-07-01 13:27:28
- date last changed
- 2024-03-13 08:10:36
@article{02c2efd4-7af1-4980-a68e-325c605cd41d,
abstract = {{<p>Glutamic acid decarboxylase (GAD) enzymes catalyse the formation of gamma-aminobuturic acid (GABA), which is a major transmittor in the central nervous system but also exerts functions in peripheral organs. Recent molecular analyses have revealed surprising new roles for the GAD isoforms in human diseases of autoimmune character including neurological disorders and insulin-dependent diabetes. In the 1995 Frontiers in Medicine Symposium, the coauthors of this review discussed the genetics, cell biology, molecular immunology and the role of GAD as autoantigens in human autoimmunity. Studies on disease diagnosis, prediction, and prognosis have revealed unique patterns of reactivities in both cellular and humoral immune responses. Further work will be needed to establish whether the GAD molecules can be used to treat autoimmune diseases.</p>}},
author = {{Lernmark, Å}},
issn = {{0954-6820}},
language = {{eng}},
month = {{01}},
number = {{5}},
pages = {{259--277}},
publisher = {{Wiley-Blackwell}},
series = {{Journal of Internal Medicine}},
title = {{Glutamic acid decarboxylase - Gene to antigen to disease}},
url = {{http://dx.doi.org/10.1046/j.1365-2796.1996.27859000.x}},
doi = {{10.1046/j.1365-2796.1996.27859000.x}},
volume = {{240}},
year = {{1996}},
}