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Collagen type II-specific monoclonal antibody-induced arthritis in mice - Description of the disease and the influence of age, sex, and genes

Nandakumar, KS; Svensson, Lars LU and Holmdahl, Rikard LU (2003) In American Journal of Pathology 163(5). p.1827-1837
Abstract
Transfer of collagen type H (CH)-specific monoclonal antibodies induces an acute form of arthritis (collagen type H antibody-induced arthritis, CAIA) in nave mice. Arthritis was induced using a pair of monoclonal antibodies M2139 and CIIC1, binding to J1 and C1(I) epitopes of CH, respectively. Thereafter, lipopolysaccharide injection was used to increase the incidence and severity of the disease. This model was used to investigate the effect of genes, age, and sex as well as effector cells in the end-stage effector phase of arthritis pathogenesis. Injection of a single monoclonal antibody induced arthritis only after lipopolysaccharide stimulation. CAIA showed differences in disease penetration among the susceptible strains indicating the... (More)
Transfer of collagen type H (CH)-specific monoclonal antibodies induces an acute form of arthritis (collagen type H antibody-induced arthritis, CAIA) in nave mice. Arthritis was induced using a pair of monoclonal antibodies M2139 and CIIC1, binding to J1 and C1(I) epitopes of CH, respectively. Thereafter, lipopolysaccharide injection was used to increase the incidence and severity of the disease. This model was used to investigate the effect of genes, age, and sex as well as effector cells in the end-stage effector phase of arthritis pathogenesis. Injection of a single monoclonal antibody induced arthritis only after lipopolysaccharide stimulation. CAIA showed differences in disease penetration among the susceptible strains indicating the importance of non-major histocompatibility complex genes on the antibody effector pathway. B-cell-deficient mice were susceptible to CAIA and in some genetic backgrounds B-cell deficiency leads to enhanced arthritis. Histology of the affected paws revealed massive infiltrations of neutrophils along with bone and cartilage erosion, pannus formation, and fibrin deposition. Depletion of neutrophils significantly reduced the incidence and severity of the disease. CAIA susceptibility increased with age. Males were more susceptible than females and estrogen treatment decreased the development of arthritis. We conclude that CAIA is an acute arthritis triggered by antibody binding and neutrophils bypassing immune activation but with many characteristics in common with collagen-induced arthritis. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
American Journal of Pathology
volume
163
issue
5
pages
1827 - 1837
publisher
American Society for Investigative Pathology
external identifiers
  • pmid:14578183
  • wos:000186148200018
  • scopus:0142213223
ISSN
1525-2191
language
English
LU publication?
yes
id
c8283d8e-ec5d-44ab-a5e3-0782ed257fed (old id 298183)
alternative location
http://ajp.amjpathol.org/cgi/content/abstract/163/5/1827
date added to LUP
2007-09-18 14:30:55
date last changed
2018-05-29 09:44:43
@article{c8283d8e-ec5d-44ab-a5e3-0782ed257fed,
  abstract     = {Transfer of collagen type H (CH)-specific monoclonal antibodies induces an acute form of arthritis (collagen type H antibody-induced arthritis, CAIA) in nave mice. Arthritis was induced using a pair of monoclonal antibodies M2139 and CIIC1, binding to J1 and C1(I) epitopes of CH, respectively. Thereafter, lipopolysaccharide injection was used to increase the incidence and severity of the disease. This model was used to investigate the effect of genes, age, and sex as well as effector cells in the end-stage effector phase of arthritis pathogenesis. Injection of a single monoclonal antibody induced arthritis only after lipopolysaccharide stimulation. CAIA showed differences in disease penetration among the susceptible strains indicating the importance of non-major histocompatibility complex genes on the antibody effector pathway. B-cell-deficient mice were susceptible to CAIA and in some genetic backgrounds B-cell deficiency leads to enhanced arthritis. Histology of the affected paws revealed massive infiltrations of neutrophils along with bone and cartilage erosion, pannus formation, and fibrin deposition. Depletion of neutrophils significantly reduced the incidence and severity of the disease. CAIA susceptibility increased with age. Males were more susceptible than females and estrogen treatment decreased the development of arthritis. We conclude that CAIA is an acute arthritis triggered by antibody binding and neutrophils bypassing immune activation but with many characteristics in common with collagen-induced arthritis.},
  author       = {Nandakumar, KS and Svensson, Lars and Holmdahl, Rikard},
  issn         = {1525-2191},
  language     = {eng},
  number       = {5},
  pages        = {1827--1837},
  publisher    = {American Society for Investigative Pathology},
  series       = {American Journal of Pathology},
  title        = {Collagen type II-specific monoclonal antibody-induced arthritis in mice - Description of the disease and the influence of age, sex, and genes},
  volume       = {163},
  year         = {2003},
}