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Well suited for study of onset and development of EAE.

Group size can be smaller (8–12 mice/group) as EAE develops in more than 90% of mice, mice show only limited recovery from EAE and disease is more uniform than in SJL mice.

The first wave of EAE usually lasts 7 to 14 days, allowing a longer time to observe differences in disease development.

Poorly suited for study of EAE relapses and therapeutics targeting B-cells.

C57BL/6 mice mostly develop chronic EAE.

Peptide-induced EAE (MOG_35-55 or MBP_1-11) has been reported to be independent of B-cell presence. [1, 2]. Because of this, peptide-induced EAE models may not be suitable for testing therapeutics aimed at B-cell depletion or impairment of B-cell function.

Recommended for testing therapeutics aimed at impairing B-cell function.

Clinical data indicates that B-cells play a pathogenic role in multiple sclerosis (MS). MS patients had reduced numbers of gadolinium-enhancing lesions over a 48-week period after B-cell depleting therapy with Rituximab [3].

B-cells have been reported as necessary to development of EAE induced by human MOG_1-125. [2, 4, 5]. It is therefore likely that MOG_1-125-induced EAE is a good model for testing therapeutics which target B-cells.

Expensive.

C57BL/6 mice mostly develop chronic EAE.

Well suited for study of EAE relapses. Most mice will recover from the first wave of EAE and 50 to 70% of mice will relapse.

EAE can be induced either with or without pertussis toxin (PTX). EAE will develop in 70% or more of mice without using PTX.

First wave is short (2 to 7 days in most mice) and less uniform compared to EAE in C57BL/6 mice.

Group size of 15 to 20 is recommended for study of relapses since relapse incidence is 50 to 70%.

Model lasts 40 days or longer when both first wave and relapses are followed.