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A genetic basis for shared autoimmunity in mouse models.

Andersson, Åsa LU and Holmdahl, Rikard LU (2005) In Autoimmunity 38(3). p.209-217
Abstract
Development of autoimmune disease is the result of activation of the immune system that subsequently leads to tissue destruction. Although the clinical outcome significantly differs between autoimmune diseases, some pathogenic pathways could be shared. During the recent years, intense efforts to find the genetic factors behind development of the complex and polygenic autoimmune diseases have been undertaken. The difficulties in addressing what genetic factors predispose for autoimmunity in humans underline the importance of animal models in the understanding of the general mechanisms behind the initiation of disease. Interestingly, it has been observed in studies of experimental models of autoimmune diseases, that many of the genetic... (More)
Development of autoimmune disease is the result of activation of the immune system that subsequently leads to tissue destruction. Although the clinical outcome significantly differs between autoimmune diseases, some pathogenic pathways could be shared. During the recent years, intense efforts to find the genetic factors behind development of the complex and polygenic autoimmune diseases have been undertaken. The difficulties in addressing what genetic factors predispose for autoimmunity in humans underline the importance of animal models in the understanding of the general mechanisms behind the initiation of disease. Interestingly, it has been observed in studies of experimental models of autoimmune diseases, that many of the genetic linkages to disease development are located in the same genetic regions and potentially could be controlled by the same gene. Furthermore, comparison of the mouse/rat genetic regions with regions of association to human inflammatory diseases, also demonstrates some homologous loci between species. Some mouse strains can develop disease in more than one model for autoimmunity. This not only argues for some general mechanisms, but it also supports mechanisms related to the specific tissues attacked in the various autoimmune diseases. Here, we will discuss some aspects of shared autoimmunity in mouse models from a genetic point of view. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Autoimmunity
volume
38
issue
3
pages
209 - 217
publisher
Taylor & Francis
external identifiers
  • wos:000230647500005
  • pmid:16126509
  • scopus:21844436251
ISSN
0891-6934
DOI
10.1080/08916930500050269
language
English
LU publication?
yes
id
2f962f93-da25-44fe-9bce-4c8c5840c07d (old id 144031)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16126509&dopt=Abstract
date added to LUP
2007-07-09 16:18:11
date last changed
2017-08-20 04:19:28
@article{2f962f93-da25-44fe-9bce-4c8c5840c07d,
  abstract     = {Development of autoimmune disease is the result of activation of the immune system that subsequently leads to tissue destruction. Although the clinical outcome significantly differs between autoimmune diseases, some pathogenic pathways could be shared. During the recent years, intense efforts to find the genetic factors behind development of the complex and polygenic autoimmune diseases have been undertaken. The difficulties in addressing what genetic factors predispose for autoimmunity in humans underline the importance of animal models in the understanding of the general mechanisms behind the initiation of disease. Interestingly, it has been observed in studies of experimental models of autoimmune diseases, that many of the genetic linkages to disease development are located in the same genetic regions and potentially could be controlled by the same gene. Furthermore, comparison of the mouse/rat genetic regions with regions of association to human inflammatory diseases, also demonstrates some homologous loci between species. Some mouse strains can develop disease in more than one model for autoimmunity. This not only argues for some general mechanisms, but it also supports mechanisms related to the specific tissues attacked in the various autoimmune diseases. Here, we will discuss some aspects of shared autoimmunity in mouse models from a genetic point of view.},
  author       = {Andersson, Åsa and Holmdahl, Rikard},
  issn         = {0891-6934},
  language     = {eng},
  number       = {3},
  pages        = {209--217},
  publisher    = {Taylor & Francis},
  series       = {Autoimmunity},
  title        = {A genetic basis for shared autoimmunity in mouse models.},
  url          = {http://dx.doi.org/10.1080/08916930500050269},
  volume       = {38},
  year         = {2005},
}