Total abrogation of collagen II-induced arthritis and the B cell response to type II collagen using suboptimal doses of a topoisomerase II antagonist.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/109918
- author
- Verdrengh, M ; Jonsson, I-M ; Zaether, O ; Bajtner, Estelle LU ; Holmdahl, Rikard LU and Tarkowski, A
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Annals of the Rheumatic Diseases
- volume
- 61
- issue
- 9
- pages
- 829 - 831
- publisher
- BMJ Publishing Group
- external identifiers
-
- wos:000177600000012
- pmid:12176810
- scopus:0036720370
- ISSN
- 1468-2060
- DOI
- 10.1136/ard.61.9.829
- 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
- f5b0cf18-2720-476a-a679-9053b9a8e1cf (old id 109918)
- alternative location
- http://ard.bmjjournals.com/cgi/content/abstract/61/9/829
- date added to LUP
- 2016-04-01 16:11:13
- date last changed
- 2022-01-28 17:55:30
@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 = {{BMJ Publishing Group}},
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 = {{https://lup.lub.lu.se/search/files/4596003/623645.pdf}},
doi = {{10.1136/ard.61.9.829}},
volume = {{61}},
year = {{2002}},
}