Skip Navigation



Rheumatology Advance Access published online on January 5, 2005

Rheumatology, doi:10.1093/rheumatology/keh477
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
44/3/299    most recent
keh477v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Loughry, A.
Right arrow Articles by Hall, F. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Loughry, A.
Right arrow Articles by Hall, F. C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

British Society for Rheumatology; all rights reserved
Received August 2, 2004
Accepted October 12, 2004

Original Papers

Inflammatory arthritis and dermatitis in thymectomized, CD25+ cell-depleted adult mice

A. Loughry 1, S. Fairchild 2, N. Athanasou 3, J. Edwards 3, and F. C. Hall 2*

1 Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK
2 Department of Clinical Medicine, Addenbrooke's Hospital, Cambridge, UK
3 Nuffield Orthopaedic Centre, Oxford, UK

* To whom correspondence should be addressed.
F. C. Hall, E-mail: fch22{at}medschl.cam.ac.uk


   Abstract

Objective. To investigate the effect of CD25+ or CTLA-4+ cell depletion on the natural history of collagen-induced and spontaneous arthritis in male DBA1/J mice.

Methods. Male DBA/1J mice were treated with anti-CD25 depleting antibody (PC61) or isotype control (GL113), or with anti-CTLA-4 depleting antibody (4F10) at various time-points peri- and post-immunization with bovine collagen type II, emulsified in adjuvant. In order to develop a model system in which long-term depletion of CD25+ regulatory T cells can be achieved prior to immunization, adult male DBA/1J mice were thymectomized prior to administration of either PC61 or GL113. An ELISA demonstrated that PC61 and GL113 antibodies were undetectable by 21 days after administration and FACS analysis confirmed the long-term depletion of CD25+ cells in peripheral blood.

Results. In the thymectomized mice treated with PC61, the CD25+ population was depleted and a spontaneous arthritis developed (P = 0.03). In the non-thymectomized mice, administration of CTLA-4-depleting antibody prior to immunization exacerbated arthritis in mice immunized with bovine collagen type II emulsified in incomplete Freund's adjuvant (P<0.01). However, no significant difference in the natural history of arthritis was evident in mice treated with CD25-depleting antibody (PC61) compared with control antibody (GL113).

Conclusions. Two separate models implicate CD25+ CTLA-4+ constitutive cells in suppression of arthritis in susceptible DBA/1 males: exacerbation of collagen-induced arthritis following CTLA-4 depletion at the start of induction and spontaneous arthritis in the thymectomy/CD25+ depletion model.

Keywords: Inflammatory arthritis; Dermatitis; CD25; Thymectomy; Mice.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
CVIHome page
D. T. Nardelli, T. F. Warner, S. M. Callister, and R. F. Schell
Anti-CD25 Antibody Treatment of Mice Vaccinated and Challenged with Borrelia spp. Does Not Exacerbate Arthritis but Inhibits Borreliacidal Antibody Production.
Clin. Vaccine Immunol., August 1, 2006; 13(8): 884 - 891.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.