Prevention and therapy with electrolectin of experimental autoimmune myasthenia gravis in rabbits.
Electrolectin (EL), an endogenous beta-D-galactoside-binding lectin from Electrophorus electricus, was found to have a prophylactic and therapeutic action on the experimental autoimmune myasthenia gravis (EAMG) in rabbits. EAMG is an autoimmune disease induced by immunization with the purified acetylcholine receptor protein (AChR) and is considered to be a good model for the human disease myasthenia gravis. Simultaneous immunization with AChR and EL completely prevented the onset of myasthenic symptoms. This preventive effect was accompanied by a decrease in the recognition of AChR by anti-AChR antibodies. The administration of EL to myasthenic rabbits led, in most cases, to a complete recovery which was not accompanied by any significant change in the level of circulating anti-AChR antibodies. No evidence for an action of EL at the muscular level could be obtained. EL, however, was found to bind to rabbit lymphocytes and to stimulate their mitosis. These results suggest that EL produces its effects on EAMG by acting at the level of the immune system. It is proposed that EL may play a role in the immunological regulation of the response to self-antigen, which could be one of the biological functions of this animal lectin.
D000371:Agglutination; D000818:Animals; D000917:Antibody Formation; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology / Q000628:therapy*; D001666:Binding Sites, Antibody; D005260:Female; D037161:Galectins; D037102:Lectins / Q000008:administration & dosage* / Q000494:pharmacology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000378:metabolism; D009157:Myasthenia Gravis / Q000209:etiology / Q000276:immunology / Q000628:therapy*; D011817:Rabbits; D011950:Receptors, Cholinergic / Q000276:immunology / Q000502:physiology
D037161:Galectins; D037102:Lectins; D011950:Receptors, Cholinergic