Key result
EAE models vary in clinical course and demyelination depending on antigen and mouse strain.
Why the study?
Experimental allergic encephalomyelitis (EAE) varies in clinical course, demyelination, and immune response depending on antigen and mouse strain, requiring focused discussion on MOG-induced EAE.
EAE model variability warrants caution in MS preclinical work; leaves open optimal standardization for translational validity.
Experimental allergic encephalomyelitis (EAE),an animal model of multiple sclerosis (MS), has traditionally been induced by injection of spinal cord and its derivatives, or by passive transfer of T cells activated against spinal cord components, into various strains of mice and rats.Mice of different genetic backgrounds vary in their susceptibility to the disease and react to different components of the myelin sheath (reviewed in Encinas et al., 1996).Regardless of antigenic challenge and mouse strain, EAE is almost always characterized by paralysis, weight loss, and a mononuclear infiltrate in the CNS.Demyelination varies depending on the antigen and the mouse strain.For instance, slight demyelination is apparent in SJL and PWJ mice immunized with myelin basic protein (MBP) or proteolipid protein (PLP) (Raine, 1997), while elctensive demyelination is found in C57BL/6 mice immunized with myelin oligodendrocyte protein (MOG) (Men-de1 et al., 1995).The clinical course of the disease varies depending on antigen and strain, from an acute monophasic disease with death or recovery, to relapsing remitting, to a chronic sustained course.In this Forum, our discussion will be focused on, but
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Hjelmström et al. (1998) conducted a review in Experimental allergic encephalomyelitis (EAE) / Multiple Sclerosis. Experimental allergic encephalomyelitis (EAE) models vary in clinical course and extent of demyelination depending on the specific antigen and mouse strain used.
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