Soluble complement receptor type 1 inhibits experimental autoimmune neuritis in Lewis rats.

Experimental autoimmune neuritis (EAN) in Lewis rats induced by immunization with bovine peripheral nerve myelin in complete Freund's adjuvant is an animal model of the human Guillain-Barré syndrome. In this study myelin-induced EAN was treated with 30 mg/kg per day human soluble complement receptor type 1 (sCR1) beginning on day 8 post immunization (p.i.). Clinical signs of disease were markedly suppressed by application of sCR1 and none of eight treated animals but seven of nine control rats developed paraparesis. Electrophysiologic examination of sciatic nerve function 13 days p.i. revealed faster nerve conduction velocities and significantly higher compound muscle action potentials in sCR1-injected animals. In sections of sciatic nerves acquired 16 days p.i. extended demyelination and axonal degeneration was prevented by treatment with sCR1 in vivo. Our findings underscore the functional importance of complement during inflammatory demyelination in the peripheral nervous system and suggest sCR1 as a potential therapeutic approach in these diseases.