Anti-C5 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease.
AUTOR(ES)
Wang, Y
RESUMO
Activated components of the complement system are potent mediators of inflammation that may play an important role in numerous disease states. For example, they have been implicated in the pathogenesis of inflammatory joint diseases including rheumatoid arthritis (RA). To target complement activation in immune-mediated joint inflammation, we have utilized monoclonal antibodies (mAbs) that inhibit the complement cascade at C5, blocking the generation of the major chemotactic and proinflammatory factors C5a and C5b-9. In this study, we demonstrate the efficacy of a mAb specific for murine C5 in the treatment of collagen-induced arthritis, an animal model for RA. We show that systemic administration of the anti-C5 mAb effectively inhibits terminal complement activation in vivo and prevents the onset of arthritis in immunized animals. Most important, anti-C5 mAb treatment is also highly effective in ameliorating established disease. These results demonstrate a critical role for activated terminal complement components not only in the induction but also in the progression of collagen-induced arthritis and suggest that C5 may be an attractive therapeutic target in RA.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=41086Documentos Relacionados
- Anti-tumor necrosis factor ameliorates joint disease in murine collagen-induced arthritis.
- Synergy between anti-CD4 and anti-tumor necrosis factor in the amelioration of established collagen-induced arthritis.
- Restricted expression of anti-type II collagen antibody isotypes in mice suppressed for collagen-induced arthritis.
- Gene therapy for established murine collagen-induced arthritis by local and systemic adenovirus-mediated delivery of interleukin-4
- Antigen-specific T cell–mediated gene therapy in collagen-induced arthritis