Anti-C5 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease - PubMed (original) (raw)

Anti-C5 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease

Y Wang et al. Proc Natl Acad Sci U S A. 1995.

Abstract

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.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Clin Exp Immunol. 1988 Sep;73(3):473-8 - PubMed
    1. J Immunol. 1989 Apr 1;142(7):2237-43 - PubMed
    1. Ann Rheum Dis. 1989 Apr;48(4):302-6 - PubMed
    1. Scand J Rheumatol Suppl. 1988;76:111-6 - PubMed
    1. Immunology. 1990 Feb;69(2):237-42 - PubMed

MeSH terms

Substances

LinkOut - more resources