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Experimental Models

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Mouse EAE Models - Overview and Model Selection

Protocols

Hooke Kits™

EAE induction – What are the advantages and disadvantages of the different models and antigens?
What is the difference between the multiple products with identical names (but different catalog numbers)?

EAE induction – What are the advantages and disadvantages of the different models and antigens?

We offer Hooke Kits™ for inducing EAE in:

C57BL/6 mice using MOG_35-55
C57BL/6 mice using MOG_1-125
SJL mice using PLP_139-151
Lewis rats using gpMBP_69-88

Each model has advantages and disadvantages as follows:

Model	Advantages	Disadvantages
MOG_35-55 in C57BL/6 mice	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.
MOG_1-125 in C57BL/6 mice	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.
PLP_139-151 in SJL mice	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.
gpMBP_69-88 in Lewis rats	Consistent disease onset and severity. Short clinical course (typically 20 days). EAE can be induced either with or without pertussis toxin (PTX). Disease will not relapse if PTX is not used. 30 to 60% of rats will experience one relapse when using PTX.	Rats are larger and more massive than mice; require larger compound amounts. Lewis rats do not usually develop demyelination. Rats do not experience chronic phase EAE with relapses.

Model

Advantages

Disadvantages

MOG_35-55
in
C57BL/6 mice

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.

MOG_1-125
in
C57BL/6 mice

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.

PLP_139-151
in
SJL mice

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.

gpMBP_69-88
in
Lewis rats

Consistent disease onset and severity. Short clinical course (typically 20 days).

EAE can be induced either with or without pertussis toxin (PTX). Disease will not relapse if PTX is not used. 30 to 60% of rats will experience one relapse when using PTX.

Rats are larger and more massive than mice; require larger compound amounts.

Lewis rats do not usually develop demyelination. Rats do not experience chronic phase EAE with relapses.

[1] Wolf SD et al, J Exp Med 184:2271 (1996)
[2] Lyons JA et al, Eur J Imm 29:3432 (1999)
[3] Hauser SL et al, NEJM 358:676 (2008)
[4] Svensson L et al, Eur J Imm 32:1939 (2002)
[5] Lyons JA et al, Eur J Imm 32:190 (2002)
[6] McFarlin DE, Blank SE, Kibler RF, J. Immunol. 1 13:712 (1974)
[7] Kardys E and Hashim GA, J Immunol 127:862 (1981)
[8] Mannie MD, Paterson PY, U'Prichard DC, Flouret G., Proc Natl Acad Sci USA 82:5515 (1985)
[9] Hashim GA, Day ED, Fredane L, Intintola P, Carvalho E, J Neurosci Res. 16(3):467-78 (1986)

What is the difference between the multiple products with identical names (but different catalog numbers)?

Hooke Emulsion Kits™ with similar names contain different amounts of killed Mycobacterium tuberculosis (Mtb), pertussis toxin (PTX), or other reagents.

The quantity of each reagent is chosen to optimize for the intended application of each Hooke Kit™ – disease induction, cellular immune response (T-cell proliferation, cytokine production), or humoral immune response (antibody production), while minimizing side effects induced by CFA.

Hooke Control Kits™ with identical names are sometimes in fact identical. In these cases multiple catalog numbers are listed to simplify ordering, and the price is the same for all identical products.

Reagent quantities are also adjusted so that each Hooke Kit™ has consistent potency, compensating for any lot-to-lot variation of kit components.