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Arthritis induced in rats with non-immunogenic adjuvants as models for rheumatoid arthritis

Holmdahl, Rikard LU ; Lorentzen, Johnny C. ; Lu, Shemin LU ; Olofsson, Peter LU ; Wester Rosenlöf, Lena LU ; Holmberg, Jens LU and Pettersson, Ulf (2001) In Immunological Reviews 184(1). p.184-202
Abstract
Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and... (More)
Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and dependent on the activation of alphabetaTCR (T-cell receptor)-expressing T cells. However, it has not been possible to link the immune response to joint antigens or other endogenous components although immunization with various cartilage proteins induce arthritis but with different pathogeneses. To unravel the mechanisms behind adjuvant-induced arthritis, a disease-oriented genetic approach is optimal. Several loci that control onset of arthritis, severity and chronicity of the disease have been identified in genetic crosses and most of these have been confirmed in congenic strains. In addition, many of these loci are found in other autoimmune models in the rat as well as associated with arthritis in mice and humans. (Less)
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; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Immunological Reviews
volume
184
issue
1
pages
184 - 202
publisher
Wiley-Blackwell
external identifiers
  • wos:000173738900016
  • scopus:0035704714
ISSN
1600-065X
DOI
10.1034/j.1600-065x.2001.1840117.x
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: Medical Inflammation Research (013212019)
id
d5caaf93-716b-4492-8932-954e71d0ec98 (old id 132632)
date added to LUP
2016-04-01 16:45:31
date last changed
2022-02-20 08:15:38
@article{d5caaf93-716b-4492-8932-954e71d0ec98,
  abstract     = {{Rat models are useful for studies of the pathogenesis of rheumatoid arthritis (RA) since rats are extraordinarily sensitive to induction of arthritis with adjuvants. Injection of not only the classical complete Freund's adjuvant but also mineral oil without mycobacteria and pure adjuvants such as pristane and squalene, induce severe arthritis in many rat strains. Models like pristane-induced arthritis in rats are optimal models for RA since they fulfill the RA criteria including a chronic relapsing disease course. Arthritogenic adjuvants like pristane, avridine, squalene and mineral oil are not immunogenic since they do not contain major histocompatibility complex (MHC) binding peptides. Nevertheless, the diseases are MHC-associated and dependent on the activation of alphabetaTCR (T-cell receptor)-expressing T cells. However, it has not been possible to link the immune response to joint antigens or other endogenous components although immunization with various cartilage proteins induce arthritis but with different pathogeneses. To unravel the mechanisms behind adjuvant-induced arthritis, a disease-oriented genetic approach is optimal. Several loci that control onset of arthritis, severity and chronicity of the disease have been identified in genetic crosses and most of these have been confirmed in congenic strains. In addition, many of these loci are found in other autoimmune models in the rat as well as associated with arthritis in mice and humans.}},
  author       = {{Holmdahl, Rikard and Lorentzen, Johnny C. and Lu, Shemin and Olofsson, Peter and Wester Rosenlöf, Lena and Holmberg, Jens and Pettersson, Ulf}},
  issn         = {{1600-065X}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{184--202}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Immunological Reviews}},
  title        = {{Arthritis induced in rats with non-immunogenic adjuvants as models for rheumatoid arthritis}},
  url          = {{https://lup.lub.lu.se/search/files/4771342/624327.pdf}},
  doi          = {{10.1034/j.1600-065x.2001.1840117.x}},
  volume       = {{184}},
  year         = {{2001}},
}