Abstract
Multiple sclerosis (MS) is the most common neurologic disease of young adults. In the recent years, our understanding on disease pathomechanisms has considerably improved and new therapies have emerged. Yet a cure for this devastating disorder is still a far cry away and human resources on ex vivo specimens are limited. More than 70 years after its first description, experimental autoimmune encephalomyelitis (EAE) remains an important tool to understand concepts of T cell mediated autoimmunity as well as the roles of the innate and the humoral immune systems. Some EAE models also well reflect mechanisms of tissue damage including demyelination, axonal injury and also cortical changes. A limitation of the classical EAE model is a neglect of CD8 T cell mediated immune mechanisms. Moreover, well characterized models for primary progressive MS or demyelination patterns involving primary oligodendrocyte dystrophy are still not available. Yet many current therapeutic concepts including glatiramer acetate or natalizumab stem from their successful first application in EAE models. New strategies include the widespread use of conditional knockout mice to understand the cell-type specific function of single genes, innovative approaches to establish models on the roles of B cells and CD8 T cells as well as on the relation of inflammation to primary degeneration. In summary, EAE models continue to play an important role in neuroimmunology thereby also stimulating research in other fields of the neurosciences and immunobiology.
Highlights
The model of experimental autoimmune encephalomyelitis (EAE) stems back from an attempt to understand the pathogenesis of post vaccinal encephalomyelitis, e.g., after rabies vaccination during the 1920s and 1930s
First immunization experiments with repeated inoculations of human spinal cord homogenate in rabbits and rhesus monkeys resulted in the first models of experimentally induced encephalomyelitis
The induction of EAE is not restricted to myelin antigens, as the disease can be elicited by astroglial antigens like S-100 or glial fibrillary acidic protein and neuronal antigens including Ma [5] or amyloid precursor protein (APP, [6])
Summary
Models of autoimmune demyelination in the central nervous system: on the way to translational medicine. Published: 21 October 2009 Experimental & Translational Stroke Medicine 2009, 1:5 doi:10.1186/2040-7378-1-5
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