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Publication Detail
Treatment of a newly established transgenic model of chronic arthritis with nondepleting anti-CD4 monoclonal antibody.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Mauri C, Chu CQ, Woodrow D, Mori L, Londei M
  • Publication date:
    15/11/1997
  • Pagination:
    5032, 5041
  • Journal:
    J Immunol
  • Volume:
    159
  • Issue:
    10
  • Status:
    Published
  • Country:
    United States
  • Print ISSN:
    0022-1767
  • Language:
    eng
  • Keywords:
    Animals, Antibodies, Monoclonal, Arthritis, Rheumatoid, CD4 Antigens, Collagen, Cytokines, Disease Models, Animal, Disease Susceptibility, Epitopes, Female, Immunoglobulin G, Lymphocyte Activation, Male, Mice, Mice, Inbred DBA, Mice, Transgenic, Receptors, Antigen, T-Cell, alpha-beta, T-Lymphocytes
Abstract
We established a novel animal model for rheumatoid arthritis (RA) by following backcrossing to DBA/1 of (SWR/J x DBA/1)F1 TCR-beta Tg mice, previously reported to be highly susceptible to collagen-induced arthritis. These mice evolved, upon collagen type II immunization, into a chronic arthritis that histopathologically resembles RA. The availability of such a model prompted us to study the role of CD4+ T cells throughout the evolution of disease. Here, we show that administration of nondepleting anti-CD4 not only prevented the evolution of disease but also treated established arthritis. Moreover, functional analyses of T cells isolated from anti-CD4-treated mice demonstrated that the mechanism of protection is not achieved by suppression of the Th1 population but is mediated by induction of collagen type II-specific T cell anergy. Our study suggests that: 1) CD4+ T cells have a fundamental role both in the induction and in the perpetuation of disease; 2) targeting T cells may be an appropriate therapeutic option; and 3) a suitable and well-balanced anti-CD4 treatment may be a valid approach to the control of RA.
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