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Total abrogation of collagen II-induced arthritis and the B cell response to type II collagen using suboptimal doses of a topoisomerase II antagonist.

Verdrengh, M; Jonsson, I-M; Zaether, O; Bajtner, Estelle LU ; Holmdahl, Rikard LU and Tarkowski, A (2002) In Annals of the Rheumatic Diseases 61(9). p.829-831
Abstract
BACKGROUND: Collagen-induced arthritis (CIA) is the most commonly used model of rheumatoid arthritis (RA). In both CIA and RA there is an increase in the cellular content of the synovium, this being dominated by macrophages. OBJECTIVE: To assess the impact of etoposide, a topoisomerase II antagonist known to induce monocyte apoptosis, on the development of CIA. METHODS: Mice were primed and booster immunised against collagen II (CII). One group of mice was treated with etoposide two days before CII immunisation and then on four consecutive days weekly until the end of the experiment. The second group of mice was injected with etoposide on four consecutive days a week starting 40 days after CII priming. The third group of mice were controls... (More)
BACKGROUND: Collagen-induced arthritis (CIA) is the most commonly used model of rheumatoid arthritis (RA). In both CIA and RA there is an increase in the cellular content of the synovium, this being dominated by macrophages. OBJECTIVE: To assess the impact of etoposide, a topoisomerase II antagonist known to induce monocyte apoptosis, on the development of CIA. METHODS: Mice were primed and booster immunised against collagen II (CII). One group of mice was treated with etoposide two days before CII immunisation and then on four consecutive days weekly until the end of the experiment. The second group of mice was injected with etoposide on four consecutive days a week starting 40 days after CII priming. The third group of mice were controls receiving phosphate buffered saline (PBS). The mice were examined for development of arthritis, numbers of circulating leucocytes, serum CII antibody, and cytokine concentrations. RESULTS: None of the mice given etoposide before CII immunisation developed arthritis. Serum concentrations of anti-CII antibodies were undetectable in these mice, whereas they displayed significantly increased concentrations of interferon gamma and interleukin 6. In addition, the CII specific B cell responses in the draining lymph nodes were highly suppressed. Also, mice treated with etoposide at the onset of clinical arthritis showed reduced frequency of their disease by 50%. CONCLUSION: There was a striking disease alleviating impact of topoisomerase II antagonist on the course of CII-induced arthritis. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Annals of the Rheumatic Diseases
volume
61
issue
9
pages
829 - 831
publisher
British Medical Association
external identifiers
  • wos:000177600000012
  • pmid:12176810
  • scopus:0036720370
ISSN
1468-2060
DOI
10.1136/ard.61.9.829
language
English
LU publication?
yes
id
f5b0cf18-2720-476a-a679-9053b9a8e1cf (old id 109918)
alternative location
http://ard.bmjjournals.com/cgi/content/abstract/61/9/829
date added to LUP
2007-07-20 08:12:35
date last changed
2017-01-01 06:58:13
@article{f5b0cf18-2720-476a-a679-9053b9a8e1cf,
  abstract     = {BACKGROUND: Collagen-induced arthritis (CIA) is the most commonly used model of rheumatoid arthritis (RA). In both CIA and RA there is an increase in the cellular content of the synovium, this being dominated by macrophages. OBJECTIVE: To assess the impact of etoposide, a topoisomerase II antagonist known to induce monocyte apoptosis, on the development of CIA. METHODS: Mice were primed and booster immunised against collagen II (CII). One group of mice was treated with etoposide two days before CII immunisation and then on four consecutive days weekly until the end of the experiment. The second group of mice was injected with etoposide on four consecutive days a week starting 40 days after CII priming. The third group of mice were controls receiving phosphate buffered saline (PBS). The mice were examined for development of arthritis, numbers of circulating leucocytes, serum CII antibody, and cytokine concentrations. RESULTS: None of the mice given etoposide before CII immunisation developed arthritis. Serum concentrations of anti-CII antibodies were undetectable in these mice, whereas they displayed significantly increased concentrations of interferon gamma and interleukin 6. In addition, the CII specific B cell responses in the draining lymph nodes were highly suppressed. Also, mice treated with etoposide at the onset of clinical arthritis showed reduced frequency of their disease by 50%. CONCLUSION: There was a striking disease alleviating impact of topoisomerase II antagonist on the course of CII-induced arthritis.},
  author       = {Verdrengh, M and Jonsson, I-M and Zaether, O and Bajtner, Estelle and Holmdahl, Rikard and Tarkowski, A},
  issn         = {1468-2060},
  language     = {eng},
  number       = {9},
  pages        = {829--831},
  publisher    = {British Medical Association},
  series       = {Annals of the Rheumatic Diseases},
  title        = {Total abrogation of collagen II-induced arthritis and the B cell response to type II collagen using suboptimal doses of a topoisomerase II antagonist.},
  url          = {http://dx.doi.org/10.1136/ard.61.9.829},
  volume       = {61},
  year         = {2002},
}