Abstract
Experimental allergic encephalomyelitis (EAE) is a T-cell-mediated auto-immune central nervous system (CNS) disease, characterized clinically by ascending paralysis and histologically by perivascular mononuclear cell inflammation of the brain and spinal cord. The methods described in this chapter have provided a highly reproducible model for investigating the cellular mechanism of auto-immune encephalomyelitis. The discovery that EAE can be transferred with relatively small numbers of activated donor lymphocytes will permit the evaluation of the cellular interactions involved in the induction of this auto-immune disease. Antigen-presenting cells, helper T cells, and interleukin play a role in the induction of EAE. The major EAE-inducing antigen in CNS tissue is myelin basis protein (BP), which represents about 30% of the total myelin protein and is an integral structural constituent of the myelin sheath. EAE can be adoptively transferred from immunized donors to syngeneic recipients with viable lymphocytes, and transfer is enhanced dramatically by culturing the donor cells in vitro in the presence of the T-cell mitogen concanavalin A 3 or BP.
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