Experimental allergic encephalomyelitis in cobra venom factor-treated and C4-deficient guinea pigs.
Experimental allergic encephalomyelitis (EAE) was studied in guinea pigs with an inherited deficiency of the fourth component of complement (C4) and in guinea pigs injected with cobra venom factor to deplete the third component and late-acting components of complement. EAE was elicited by immunization with homologous spinal cord or purified basic protein. Administration of cobra factor after the injection of encephalitogenic emulsion delayed the onset and reduced the intensity of the clinical manifestations of EAE. In addition, cobra factor markedly reduced mortality during the sixty days of observation. However, pathological changes of perivascular infiltration and demyelination were similar in cobra factor-treated and untreated animals. Clinical signs of EAE an mortality in C4-deficient guinea pigs were no different from those in normocomplementemic controls. Thus, although activation of the classic complement pathway does not appear to be involved in the production of EAE in guinea pigs, our results suggest a possible role of the alternative complement pathway in the pathogenesis of EAE.
D000818:Animals; D001324:Autoantigens; D003176:Complement C3 / Q000037:antagonists & inhibitors; D003181:Complement C4 / Q000172:deficiency*; D004546:Elapid Venoms / Q000494:pharmacology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D005260:Female; D006168:Guinea Pigs; D004676:Myelin Basic Protein / Q000276:immunology; D013116:Spinal Cord / Q000276:immunology
D001324:Autoantigens; D003176:Complement C3; D003181:Complement C4; D004546:Elapid Venoms; D004676:Myelin Basic Protein