eae

Experimental autoimmune encephalomyelitis (EAE) is an animal model used to study inflammatory demyelinating diseases of the central nervous system, most notably multiple sclerosis (MS). It is induced in various species to reproduce immune-mediated CNS damage and to explore disease mechanisms and potential therapies.

EAE is commonly produced by active immunization with self-myelin antigens, such as myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), or proteolipid protein (PLP), emulsified in adjuvants like Complete Freund's adjuvant and often accompanied by pertussis toxin to enhance CNS permeability and disease onset. There are also adoptive transfer models, in which encephalitogenic T cells are generated in donor animals and transferred into recipients.

Pathologically, EAE features immune cell infiltration, demyelination, and axonal injury within the CNS, with clinical signs that vary by species and protocol. In mice and rats, signs include tail weakness, hindlimb weakness or paralysis, spasticity, and ataxia. The disease course can be monophasic, relapsing-remitting, or chronic depending on the model.

EAE serves as a platform to investigate MS pathogenesis, including T cell- and B cell-mediated mechanisms, cytokine networks, and the role of the blood-brain barrier. It is used to evaluate immunomodulatory therapies such as interferon, glatiramer acetate, monoclonal antibodies, and agents promoting remyelination or neuroprotection, prior to human trials.

Limitations include differences between EAE and MS in etiology, pathology, and progression. No single model captures the full complexity of MS, and results may not always translate to humans. Protocols vary by species, strain, and antigen, and animal welfare considerations are central to EAE research.

EAE was first described in the 1930s by Thomas Rivers and colleagues as an experimental model of demyelinating disease; over subsequent decades it was refined into multiple active and passive immunization models to mirror different MS aspects.