SOLUBLE COMPLEMENT RECEPTOR-1 (SCR1) PROTECTS AGAINST EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS

The loss of muscle function seen in myasthenia gravis and in the anima l model of the disease, experimental autoimmune myasthenia gravis (EAM G) is in part due to the activation of complement by anti-acetylcholin e receptor (AChR) antibodies at the motor end-plate. In this study we describe the effects of a soluble recombinant form of human complement receptor 1 (sCR1) on the development of clinical disease and receptor loss in EAMG induced passively by administration of anti-AChR antibod ies. Daily intraperitoneal injection of sCR1 significantly reduced the weight loss and severity of clinical symptoms seen and allowed treate d animals to recover normal muscle function. These data suggest that s CR1 could provide a useful additional therapeutic agent in myasthenia.