Soluble complement receptor one (sCR1) inhibits the development and progression of rat collagen-induced arthritis

We set out to determine whether inhibition of complement using sCR1 could i nfluence the development and progression of collagen arthritis in the Lewis rat. Collagen arthritis was successfully established in the Lewis rat, usi ng a novel immunization schedule. In separate experiments, cobra venom fact or (CVF) and sCR1 were used to achieve systemic complement inhibition. Thei r respective effects on disease onset and on the progression of established disease compared with saline-treated control animals was explored. Arthrit is was assessed by measurement of clinical score, paw diameter and paw volu me. Complement inhibition using either CVF or sCR1, prior to the onset of c linical signs of inflammation, delayed the development of disease. CVF was ineffective in the treatment of established disease, whereas sCR1 delayed t he progression of disease in affected joints and prevented the recruitment of further joints while the animals were complement-depleted. In the contro l saline-treated groups the disease continued to progress relentlessly. We conclude that complement activation is important in the initiation and main tenance of inflammation in collagen arthritis. The potent disease-modulatin g effect of sCR1 provides persuasive evidence that specific complement inhi biting agents may be an effective approach to the treatment of inflammatory joint diseases.