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Modelling MS: Chronic-Relapsing EAE in the NOD/Lt Mouse Strain
Phuc T Dang1, Quyen Bui1, Claretta S D'Souza1
1Department of Biochemistry and La Trobe Institute for Molecular Science, La Trobe University, Bundoora, VIC, 3086, Australia.
Abstract:
Modelling complex disorders presents considerable challenges, and multiple sclerosis (MS) is no exception to this rule. The aetiology of MS is unknown, and its pathophysiology is poorly understood. Moreover, the last two decades have witnessed a dramatic revision of the long-held view of MS as an inflammatory demyelinating white matter disease. Instead, it is now regarded as a global central nervous system (CNS) disorder with a neurodegenerative component. Currently, there is no animal model recapitulating MS immunopathogenesis. Available models are based on autoimmune-mediated demyelination, denoted experimental autoimmune encephalomyelitis (EAE) or virally or chemically induced demyelination. Of these, the EAE model has been the most commonly used. It has been extensively improved since its first description and now exists as a number of variants, including genetically modified and humanized versions. Nonetheless, EAE is a distinct disease, and each variant models only certain facets of MS. Whilst the search for more refined MS models must continue, it is important to further explore where mechanisms underlying EAE provide proof-of-principle for those driving MS pathogenesis. EAE variants generated with the myelin component myelin oligodendrocyte glycoprotein (MOG) have emerged as the preferred ones, because in this particular variant disease is associated with both T- and B-cell effector mechanisms, together with demyelination. MOG-induced EAE in the non-obese diabetic (NOD) mouse strain exhibits a chronic-relapsing EAE clinical profile and high disease incidence. We describe the generation of this variant, its contribution to the understanding of MS immune and pathogenetic mechanisms and potential for evaluation of candidate therapies.
Insights
Developing a new multiple sclerosis (MS) model using myelin oligodendrocyte glycoprotein (MOG) in NOD mice offers insights into MS pathogenesis. This model aids in understanding immune mechanisms and evaluating therapies for this complex CNS disorder.
Area of Science:
- Neuroimmunology
- Central Nervous System (CNS) Disorders
- Animal Models of Disease
Background:
- Multiple sclerosis (MS) is a complex CNS disorder with unknown etiology and poorly understood pathophysiology, shifting from an inflammatory demyelinating view to a global disorder with neurodegeneration.
- Current animal models, primarily experimental autoimmune encephalomyelitis (EAE), are based on autoimmune-mediated demyelination and do not fully recapitulate MS immunopathogenesis.
- Existing EAE variants model only specific aspects of MS, highlighting the need for refined models to understand disease mechanisms.
Purpose of the Study:
- To describe the generation of a novel multiple sclerosis (MS) model using myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in non-obese diabetic (NOD) mice.
- To explore the utility of this MOG-induced EAE variant in understanding MS immune and pathogenetic mechanisms.
- To evaluate the potential of this refined MS model for assessing candidate therapies.
Main Methods:
- Generation of a specific variant of experimental autoimmune encephalomyelitis (EAE) using myelin oligodendrocyte glycoprotein (MOG) as the antigen.
- Utilizing the non-obese diabetic (NOD) mouse strain to induce a chronic-relapsing EAE clinical profile.
- Characterization of disease incidence and associated effector mechanisms, including T- and B-cell responses and demyelination.
Main Results:
- The MOG-induced EAE model in NOD mice exhibits a chronic-relapsing clinical course, closely mimicking aspects of MS.
- This model demonstrates the involvement of both T-cell and B-cell effector mechanisms in disease pathogenesis, alongside demyelination.
- The variant shows a high disease incidence, making it suitable for mechanistic studies and therapeutic evaluations.
Conclusions:
- The MOG-induced EAE model in NOD mice provides a valuable tool for investigating the complex immune and pathogenetic mechanisms of multiple sclerosis (MS).
- This model serves as a proof-of-principle for exploring disease drivers relevant to MS pathogenesis.
- The chronic-relapsing nature and high incidence of this EAE variant make it a promising platform for the evaluation of novel MS therapies.
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