title: Soluble complement receptor 1 (sCR1) protects against experimental autoimmune myasthenia gravis.
abstract: The loss of muscle function seen in myasthenia gravis and in the animal model of the disease, experimental autoimmune myasthenia gravis (EAMG) is in part due to the activation of complement by anti-acetylcholine 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 antibodies. Daily intraperitoneal injection of sCR1 significantly reduced the weight loss and severity of clinical symptoms seen and allowed treated animals to recover normal muscle function. These data suggest that sCR1 could provide a useful additional therapeutic agent in myasthenia.
authors.affiliation: Department of Medical Biochemistry, University of Wales College of Medicine, Heath Park, Cardiff, UK. wmbsjp@cardiff.ac.uk
authors.forename: S J
authors.initials: SJ
authors.lastname: Piddlesden
authors.forename: S
authors.initials: S
authors.lastname: Jiang
authors.forename: J L
authors.initials: JL
authors.lastname: Levin
authors.forename: A
authors.initials: A
authors.lastname: Vincent
authors.forename: B P
authors.initials: BP
authors.lastname: Morgan
mesh_terms: D000818:Animals; D005260:Female; D009132:Muscles / Q000378:metabolism; D009157:Myasthenia Gravis / Q000628:therapy*; D051381:Rats; D011917:Rats, Inbred Lew; D017463:Receptors, Complement 3b / Q000276:immunology*; D011978:Receptors, Nicotinic / Q000378:metabolism; D012995:Solubility
chemical_list: D017463:Receptors, Complement 3b; D011978:Receptors, Nicotinic