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Genetic control of collagen-induced arthritis in a cross with NOD and C57Bl/10 mice is dependent on gene regions coding for complement factor 5 and FcγRIIb and is not associated with loci controlling diabetes.

Johansson, Åsa LU ; Sundler, Martin ; Kjellen, Peter ; Johannesson, Martina LU ; Cook, Andrew ; Lindqvist, Anna-Karin B. ; Nakken, Britt ; Bolstad, Anne Isine ; Skarstein, Kathrine and Holmdahl, Rikard (2001) In European Journal of Immunology 31(6). p.1847-1856
Abstract
The nonobese diabetic (NOD) mouse spontaneously develops autoimmune-mediated diseases such as diabetes and Sjögren′s syndrome. To investigate whether NOD genes also promote autoimmune-mediatedarthritis we established a NOD strain with an MHC class II fragment containing the Aq class II gene predisposing for collagen induced arthritis (NOD.Q). However, this mouse was resistant to arthritis in contrast to other Aq expressing strains such as B10.Q and DBA/1. To determine the major resistance factor/s, a genetic analysis was performed. (NOD.Q×B10.Q)F1 mice were resistant, whereas 27% of the (NOD.Q×B10.Q)F2 mice developed severe arthritis. Genetic mapping of 353 F2 mice revealed two loci associated with arthritis. One locus was found on... (More)
The nonobese diabetic (NOD) mouse spontaneously develops autoimmune-mediated diseases such as diabetes and Sjögren′s syndrome. To investigate whether NOD genes also promote autoimmune-mediatedarthritis we established a NOD strain with an MHC class II fragment containing the Aq class II gene predisposing for collagen induced arthritis (NOD.Q). However, this mouse was resistant to arthritis in contrast to other Aq expressing strains such as B10.Q and DBA/1. To determine the major resistance factor/s, a genetic analysis was performed. (NOD.Q×B10.Q)F1 mice were resistant, whereas 27% of the (NOD.Q×B10.Q)F2 mice developed severe arthritis. Genetic mapping of 353 F2 mice revealed two loci associated with arthritis. One locus was found on chromosome 2 (LOD score 9.8), at the location of the complement factor 5 (C5) gene. The susceptibility allele was from B10.Q, which contains a productive C5 encoding gene in contrast to NOD.Q. The other significant locus was found on chromosome 1 (LOD score 5.6) close to the Fc-gamma receptor IIb gene, where NOD carried the susceptible allele. An interaction between the two loci was observed, indicating that they operate on the same or on interacting pathways. The genetic control of arthritis is unique in comparison to diabetes, since none of these loci have been identified in analysis of diabetes susceptibility. (Less)
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author
; ; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
European Journal of Immunology
volume
31
issue
6
pages
1847 - 1856
publisher
John Wiley & Sons Inc.
ISSN
1521-4141
DOI
10.1002/1521-4141(200106)31:6<1847::AID-IMMU1847>3.0.CO;2-F
language
English
LU publication?
yes
id
76665c18-c8bf-42f2-9312-6c7d4d95b4b3
date added to LUP
2024-06-05 10:59:04
date last changed
2024-06-05 13:24:41
@article{76665c18-c8bf-42f2-9312-6c7d4d95b4b3,
  abstract     = {{The nonobese diabetic (NOD) mouse spontaneously develops autoimmune-mediated diseases such as diabetes and Sjögren′s syndrome. To investigate whether NOD genes also promote autoimmune-mediatedarthritis we established a NOD strain with an MHC class II fragment containing the Aq class II gene predisposing for collagen induced arthritis (NOD.Q). However, this mouse was resistant to arthritis in contrast to other Aq expressing strains such as B10.Q and DBA/1. To determine the major resistance factor/s, a genetic analysis was performed. (NOD.Q×B10.Q)F1 mice were resistant, whereas 27% of the (NOD.Q×B10.Q)F2 mice developed severe arthritis. Genetic mapping of 353 F2 mice revealed two loci associated with arthritis. One locus was found on chromosome 2 (LOD score 9.8), at the location of the complement factor 5 (C5) gene. The susceptibility allele was from B10.Q, which contains a productive C5 encoding gene in contrast to NOD.Q. The other significant locus was found on chromosome 1 (LOD score 5.6) close to the Fc-gamma receptor IIb gene, where NOD carried the susceptible allele. An interaction between the two loci was observed, indicating that they operate on the same or on interacting pathways. The genetic control of arthritis is unique in comparison to diabetes, since none of these loci have been identified in analysis of diabetes susceptibility.}},
  author       = {{Johansson, Åsa and Sundler, Martin and Kjellen, Peter and Johannesson, Martina and Cook, Andrew and Lindqvist, Anna-Karin B. and Nakken, Britt and Bolstad, Anne Isine and Skarstein, Kathrine and Holmdahl, Rikard}},
  issn         = {{1521-4141}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1847--1856}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{European Journal of Immunology}},
  title        = {{Genetic control of collagen-induced arthritis in a cross with NOD and C57Bl/10 mice is dependent on gene regions coding for complement factor 5 and FcγRIIb and is not associated with loci controlling diabetes.}},
  url          = {{http://dx.doi.org/10.1002/1521-4141(200106)31:6<1847::AID-IMMU1847>3.0.CO;2-F}},
  doi          = {{10.1002/1521-4141(200106)31:6<1847::AID-IMMU1847>3.0.CO;2-F}},
  volume       = {{31}},
  year         = {{2001}},
}