Experimental Autoimmune Encephalitis (EAE)

An experimental mouse model of Multiple Sclerosis (MS)

EAE shares many clinical and pathological similarities with MS. The two conditions have a related disease course that consists of neurodegeneration resulting in progressive disability. EAE is a chronic inflammatory condition characterized by the demyelination of the CNS, involving autoimmune CD4+ Th1 cells. To induce EAE, mice are immunized with an emulsion that contains a specific myelin protein fragment (antigen) needed to trigger the expansion and differentiation of myelin protein-reactive autoimmune T-cells that target and attack the myelin proteins on neurons in the CNS. Dendritic cells in tissues pick up this antigen and take it to the lymphatic system where T-cells are primed. These T-cells eventually travel to the CNS where they mediate an attack that de-myelinates axons, slowing and disrupting the transmission of neural signals. The MOG 35-55 chronic EAE model below is useful in screening novel therapeutics for efficacy in the treatment of MS.

Chronic Model: MOG 35-55

MOG is a glycoprotein important in the myelination process of the axon. When 10-week old female C57BL/6 mice are immunized with myelin oligodendrocyte protein fragment 35-55 (MOG 35-55) they develop chronic paralysis within 8-14 days that is not characterized by a remission period.


Preclinical Drug Efficacy Studies


Mice (C57BL/6, Female, 10-weeks old)

Basic Methodology

Mice are immunized with injections of the MOG/CFA emulsion followed two-hours later by the administration of pertussis toxin. On Day 2, mice receive another injection of pertussis toxin. Mice are weighed and scored daily starting on Day 7 and continuing until the completion of the study (between 21-40 days). Length of study is determined by clinical response and is at the discretion of the investigator and/or sponsor. The administration of compounds is performed as set-forth in the study protocol.


Clinical scoring of EAE disease severity, body weights, spinal column histopathology, immunohistochemistry, and cytokine profiling using ELISA and Luminex mulitplex assays

Reference Substance(s):


Literature References:

BL McRae, CL Vanderlugt, MC Dal Canto, and SD Miller. (1995) Functional evidence for epitope spreading in the relapsing pathology of experimental autoimmune encephalomyelitis. J. Exp. Med; 182: 75 – 85.

Roberto Furlan, Alessandra Bergami, Daniela Cantarella, Elena Brambilla, Masaro Taniguchi,Paolo Dellabona, Giulia Casorati, Gianvito Martino. (2003) Activation of invariant NKT cells by GalCer administration protects mice from MOG35-55-induced EAE: critical roles for administration route and IFN- γ Eur. J. Immunology; 33: 1830–1838.

Itzhack Mendel, Nicole Kerlero de Rosbo, Avraham Ben-Nun. (1995) a myelin oligodendrocyte glycoprotein peptide induces typical chronic experimental autoimmune encephalomyelitis in H-2b mice: Fine specificity and T cell receptor V expression of encephalitogenic T cells. Eur. J. Immunology; 25: 1951-59.