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Gene-environment interactions in the aetiology of systemic lupus erythematosus

Jönsen, Andreas LU ; Bengtsson, Anders LU ; Nived, Ola LU ; Truedsson, Lennart LU and Sturfelt, Gunnar LU (2007) In Autoimmunity 40(8). p.613-617
Abstract
Systemic lupus erythematosus (SLE) is a disease that displays a multitude of symptoms and a vast array of autoantibodies. The disease course may vary substantially between patients. The current understanding of SLE aetiology includes environmental factors acting on a genetically prone individual during an undetermined time period resulting in autoimmunity and finally surpassing that individual's disease threshold. Genetic differences and environmental factors may interact specifically in the pathogenetic processes and may influence disease development and modify the disease course. Identification of these factors and their interactions in the pathogenesis of SLE is vital in understanding the disease and may contribute to identify new... (More)
Systemic lupus erythematosus (SLE) is a disease that displays a multitude of symptoms and a vast array of autoantibodies. The disease course may vary substantially between patients. The current understanding of SLE aetiology includes environmental factors acting on a genetically prone individual during an undetermined time period resulting in autoimmunity and finally surpassing that individual's disease threshold. Genetic differences and environmental factors may interact specifically in the pathogenetic processes and may influence disease development and modify the disease course. Identification of these factors and their interactions in the pathogenesis of SLE is vital in understanding the disease and may contribute to identify new treatment targets and perhaps also aid in disease prevention. However, there are several problems that need to be overcome, such as the protracted time frame of environmental influence, time dependent epigenetic alterations and the possibility that different pathogenetic pathways may result in a similar disease phenotype. This is mirrored by the relatively few studies that suggest specific gene-environment interactions. These include an association between SLE diagnosis and glutathion S-transferase gene variants combined with occupational sun exposure as well as variants of the N-acetyl transferase gene in combination with either aromatic amine exposure or hydralazine. With increased knowledge on SLE pathogenesis, the role of environmental factors and their genetic interactions may be further elucidated. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
environment, epigenetics, genetics, SLE, etiology
in
Autoimmunity
volume
40
issue
8
pages
613 - 617
publisher
Taylor & Francis
external identifiers
  • wos:000251606200008
  • pmid:18075795
  • scopus:37449019207
ISSN
0891-6934
DOI
10.1080/08916930701511051
language
English
LU publication?
yes
id
b80b0013-d764-45f5-a3f5-2bcbf94938a6 (old id 966184)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18075795?dopt=Abstract
date added to LUP
2008-01-29 15:59:58
date last changed
2017-10-22 03:40:05
@article{b80b0013-d764-45f5-a3f5-2bcbf94938a6,
  abstract     = {Systemic lupus erythematosus (SLE) is a disease that displays a multitude of symptoms and a vast array of autoantibodies. The disease course may vary substantially between patients. The current understanding of SLE aetiology includes environmental factors acting on a genetically prone individual during an undetermined time period resulting in autoimmunity and finally surpassing that individual's disease threshold. Genetic differences and environmental factors may interact specifically in the pathogenetic processes and may influence disease development and modify the disease course. Identification of these factors and their interactions in the pathogenesis of SLE is vital in understanding the disease and may contribute to identify new treatment targets and perhaps also aid in disease prevention. However, there are several problems that need to be overcome, such as the protracted time frame of environmental influence, time dependent epigenetic alterations and the possibility that different pathogenetic pathways may result in a similar disease phenotype. This is mirrored by the relatively few studies that suggest specific gene-environment interactions. These include an association between SLE diagnosis and glutathion S-transferase gene variants combined with occupational sun exposure as well as variants of the N-acetyl transferase gene in combination with either aromatic amine exposure or hydralazine. With increased knowledge on SLE pathogenesis, the role of environmental factors and their genetic interactions may be further elucidated.},
  author       = {Jönsen, Andreas and Bengtsson, Anders and Nived, Ola and Truedsson, Lennart and Sturfelt, Gunnar},
  issn         = {0891-6934},
  keyword      = {environment,epigenetics,genetics,SLE,etiology},
  language     = {eng},
  number       = {8},
  pages        = {613--617},
  publisher    = {Taylor & Francis},
  series       = {Autoimmunity},
  title        = {Gene-environment interactions in the aetiology of systemic lupus erythematosus},
  url          = {http://dx.doi.org/10.1080/08916930701511051},
  volume       = {40},
  year         = {2007},
}