Delayed, relapsing experimental allergic encephalomyelitis in mice.

Abstract

Immunization of female SJL mice with an emulsion of lyophilized mouse spinal cord, pertussis vaccine, and complete Freund's adjuvant produces a delayed and often relapsing form of experimental allergic encephalomyelitis (DR-EAE). The mice develop initial signs of disease an average of 6 mo after immunization. Relapses occurred 2 wk to 11 mo after the initial illness. Some animals had multiple relapses. Pathologic examination of the brain and spinal cord revealed perivascular infiltration of mononuclear cells with acute demyelination. Areas of subacute and chronic demyelination ("plaques") were also seen. This model produces a clinical course of relapsing-remitting disease with pathologic evidence of both recent and old inflammatory lesions at various levels of the central nervous system. It thus more closely resembles multiple sclerosis than acute EAE.

Experimental Autoimmune Encephalomyelitis in the Mouse

“…Genetic control of susceptibility to murine EAE is complex and involves genes located both within and outside of the major histocompatibility complex (MHC), and differs with the different myelin proteins used for disease induction (Andersson and Karlsson, 2004). In mouse spinal cord homogenate (MSCH)induced EAE, genes governing sensitization to histamine and other vasoactive amines (Linthicum and Frelinger, 1982;Lublin, 1982;Gonatas et al, 1986) and other unmapped genes (Montgomery and Rauch, 1982;Munoz and Mackay, 1984;Knobler et al, 1985) influence susceptibility. Susceptibility to acute EAE induced by intact MBP maps to the I-A subregion of the murine H-2 complex (Fritz et al, 1984).…”

Experimental Autoimmune Encephalomyelitis in the Mouse

“…Genetic control of susceptibility to murine EAE is complex and involves genes located both within and outside of the major histocompatibility complex (MHC) and differs with the different myelin proteins used for disease induction (Andersson and Karlsson, 2004). In mouse spinal cord homogenate (MSCH)induced EAE, genes governing sensitization to histamine and other vasoactive amines (Linthicum and Frelinger, 1982;Lublin, 1982;Gonatas et al, 1986) and other unmapped genes (Montgomery and Rauch, 1982;Munoz and Mackay, 1984;Knobler et al, 1985) influence susceptibility. Susceptibility to acute EAE induced by intact MBP maps to the I-A subregion of the murine H-2 complex Pettinelli and McFarlin (1981), Pettinelli et al (1982), Miller et al (1991), McRae et al (1992, Fritz and Zhao (1994), Segal et al (1994), Skundric et al (1993Skundric et al ( , 1994, and Tuohy and Thomas (1995).…”