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A comparative genetic analysis between collagen-induced arthritis and pristane-induced arthritis.

Olofsson, Peter; Lu, Shemin LU ; Holmberg, Jens LU ; Song, Tusheng; Wernhoff, Patrik LU ; Pettersson, Ulf and Holmdahl, Rikard LU (2003) In Arthritis and Rheumatism 48(8). p.2332-2342
Abstract
Objective

To compare the genetic regulation of collagen-induced arthritis (CIA) with that of pristane-induced arthritis (PIA) in rats.



Methods

A genome-wide linkage analysis of an (E3 × DA)DA backcross of rats with CIA (n = 364 male rats; the same strain combinations as previously used to determine the genetic control of PIA) was performed. The strongest loci in both CIA and PIA (i.e., Cia12/Pia4 and Cia13/Pia7) were isolated in congenic strains. Susceptibility in both congenic strains was tested in rats with CIA and in rats with PIA.



Results

We found a striking, although not complete, similarity of the arthritis-controlling loci in CIA and in PIA, as well as the previously... (More)
Objective

To compare the genetic regulation of collagen-induced arthritis (CIA) with that of pristane-induced arthritis (PIA) in rats.



Methods

A genome-wide linkage analysis of an (E3 × DA)DA backcross of rats with CIA (n = 364 male rats; the same strain combinations as previously used to determine the genetic control of PIA) was performed. The strongest loci in both CIA and PIA (i.e., Cia12/Pia4 and Cia13/Pia7) were isolated in congenic strains. Susceptibility in both congenic strains was tested in rats with CIA and in rats with PIA.



Results

We found a striking, although not complete, similarity of the arthritis-controlling loci in CIA and in PIA, as well as the previously defined loci associated with cartilage destruction, antibody production, and the acute-phase response. All major PIA quantitative trait loci (QTLs) identified in early severe arthritis were also strong regulators of CIA. The 2 strongest QTLs, Cia12/Pia4 on chromosome 12 and Cia13/Pia7 on chromosome 4, were also analyzed in congenic strains with DA or E3 as the background genome. Consistent with the results of linkage analysis, the congenic strain experiments showed that the chromosome 4 locus was more penetrant in CIA than in PIA, while the chromosome 12 locus almost completely dominated the control of PIA severity.



Conclusion

The underlying genetic control of CIA was found to have many, but not all, pathogenic mechanisms in common with PIA, despite the use of a cartilage-specific antigen (type II collagen) to induce CIA but not PIA. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Arthritis and Rheumatism
volume
48
issue
8
pages
2332 - 2342
publisher
John Wiley & Sons
external identifiers
  • wos:000184585000031
  • pmid:12905489
  • scopus:0041653312
ISSN
1529-0131
DOI
language
English
LU publication?
yes
id
2a3aabf7-2f87-46fa-8f0a-2ca88960ff3f (old id 117458)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12905489&dopt=Abstract
date added to LUP
2007-06-26 11:41:49
date last changed
2018-05-29 11:36:19
@article{2a3aabf7-2f87-46fa-8f0a-2ca88960ff3f,
  abstract     = {Objective<br/><br>
To compare the genetic regulation of collagen-induced arthritis (CIA) with that of pristane-induced arthritis (PIA) in rats.<br/><br>
<br/><br>
Methods<br/><br>
A genome-wide linkage analysis of an (E3 × DA)DA backcross of rats with CIA (n = 364 male rats; the same strain combinations as previously used to determine the genetic control of PIA) was performed. The strongest loci in both CIA and PIA (i.e., Cia12/Pia4 and Cia13/Pia7) were isolated in congenic strains. Susceptibility in both congenic strains was tested in rats with CIA and in rats with PIA.<br/><br>
<br/><br>
Results<br/><br>
We found a striking, although not complete, similarity of the arthritis-controlling loci in CIA and in PIA, as well as the previously defined loci associated with cartilage destruction, antibody production, and the acute-phase response. All major PIA quantitative trait loci (QTLs) identified in early severe arthritis were also strong regulators of CIA. The 2 strongest QTLs, Cia12/Pia4 on chromosome 12 and Cia13/Pia7 on chromosome 4, were also analyzed in congenic strains with DA or E3 as the background genome. Consistent with the results of linkage analysis, the congenic strain experiments showed that the chromosome 4 locus was more penetrant in CIA than in PIA, while the chromosome 12 locus almost completely dominated the control of PIA severity.<br/><br>
<br/><br>
Conclusion<br/><br>
The underlying genetic control of CIA was found to have many, but not all, pathogenic mechanisms in common with PIA, despite the use of a cartilage-specific antigen (type II collagen) to induce CIA but not PIA.},
  author       = {Olofsson, Peter and Lu, Shemin and Holmberg, Jens and Song, Tusheng and Wernhoff, Patrik and Pettersson, Ulf and Holmdahl, Rikard},
  issn         = {1529-0131},
  language     = {eng},
  number       = {8},
  pages        = {2332--2342},
  publisher    = {John Wiley & Sons},
  series       = {Arthritis and Rheumatism},
  title        = {A comparative genetic analysis between collagen-induced arthritis and pristane-induced arthritis.},
  url          = {http://dx.doi.org/},
  volume       = {48},
  year         = {2003},
}