A genetic basis for shared autoimmunity in mouse models.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/144031
- author
- Andersson, Åsa LU and Holmdahl, Rikard LU
- organization
- publishing date
- 2005
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Department of Experimental Medical Science (013210000), Medical Inflammation Research (013212019)
- 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
- 2016-04-01 15:52:31
- date last changed
- 2022-04-22 18:00:06
@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}},
doi = {{10.1080/08916930500050269}},
volume = {{38}},
year = {{2005}},
}