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Updated: Jun 20, 2026
Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
Published on: July 4, 2007
Characterization of relapsing-remitting and chronic forms of experimental autoimmune encephalomyelitis in C57BL/6
Jennifer L Berard1, Kevin Wolak, Sylvie Fournier
1Center for Research in Neuroscience, The Research Institute of the McGill University Health Center, Montreal, Quebec, Canada.
Abstract:
Multiple sclerosis (MS) is an autoimmune, demyelinating disease of the central nervous system (CNS). Like MS, the animal model experimental autoimmune encephalomyelitis (EAE) is characterized by CNS inflammation and demyelination and can follow a relapsing-remitting (RR) or chronic (CH) disease course. The molecular and pathological differences that underlie these different forms of EAE are not fully understood. We have compared the differences in RR- and CH-EAE generated in the same mouse strain (C57BL/6) using the same antigen. At the peak of disease when mice in both groups have similar clinical scores, CH-EAE is associated with increased lesion burden, myelin loss, axonal damage, and chemokine/cytokine expression when compared with RR-EAE. We further showed that inflammation and myelin loss continue to worsen in later stages of CH-EAE, whereas these features are largely resolved at the equivalent stage in RR-EAE. Additionally, axonal loss at these later stages is more severe in CH-EAE than in RR-EAE. We also demonstrated that CH-EAE is associated with a greater predominance of CD8(+) T cells in the CNS that exhibit MOG(35-55) antigen specificity. These studies therefore showed that, as early as the peak stage of disease, RR- and CH-EAE differ remarkably in their immune cell profile, chemokine/cytokine responses, and histopathological features. These data also indicated that this model of CH-EAE exhibits pathological features of a chronic-progressive disease profile and suggested that the sustained chronic phenotype is due to a combination of axonal loss, myelin loss, and continuing inflammation.
Insights
Chronic experimental autoimmune encephalomyelitis (EAE) shows greater inflammation, myelin loss, and axonal damage than relapsing-remitting EAE. This chronic EAE model exhibits progressive disease features, differing significantly from the relapsing form.
Area of Science:
- Neuroimmunology
- Central Nervous System (CNS) Diseases
- Autoimmune Disorders
Background:
- Multiple sclerosis (MS) is a CNS autoimmune demyelinating disease.
- Experimental autoimmune encephalomyelitis (EAE) is an animal model for MS, exhibiting relapsing-remitting (RR) or chronic (CH) disease courses.
- Molecular and pathological distinctions between RR-EAE and CH-EAE remain unclear.
Purpose of the Study:
- To compare the immunological and pathological differences between RR-EAE and CH-EAE in C57BL/6 mice.
- To elucidate the underlying mechanisms contributing to the chronic disease phenotype in EAE.
Main Methods:
- Induction of RR- and CH-EAE in C57BL/6 mice using the same myelin oligodendrocyte glycoprotein (MOG) antigen.
- Comparative analysis of clinical scores, lesion burden, myelin and axonal damage, and chemokine/cytokine expression at peak and later disease stages.
- Immunophenotyping of CNS-infiltrating T cells, including antigen specificity (MOG35-55).
Main Results:
- CH-EAE exhibited increased lesion burden, myelin loss, axonal damage, and chemokine/cytokine expression compared to RR-EAE at peak disease.
- Inflammation and myelin loss persisted and worsened in later stages of CH-EAE, unlike the resolution seen in RR-EAE.
- CH-EAE showed more severe axonal loss and a predominance of MOG(35-55) antigen-specific CD8(+) T cells in the CNS.
Conclusions:
- RR-EAE and CH-EAE display distinct immune cell profiles, cytokine responses, and histopathological features early in the disease course.
- The CH-EAE model demonstrates pathological characteristics of a chronic-progressive neurological condition.
- Sustained chronic EAE phenotype likely results from combined axonal loss, myelin loss, and persistent inflammation.
