Animal models

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Abstract
Different models of experimental autoimmune encephalomyelitis (EAE) have been successfully applied to investigate and manifold aspects of the autoimmune pathogenesis of multiple sclerosis. Studies using myelin‐specific T‐cell lines that transfer EAE to naive recipient animals established that only activated lymphocytes are able to cross the endothelial blood–brain barrier and cause autoimmune disease within the local parenchyma. All encephalitogenic T cells are CD4+ Th1‐type lymphocytes that recognize autoantigenic peptides in the context of MHC class II molecules. In the case of myelin basic protein (MBP) specific EAE in the Lewis rat, the T‐cell response is directed against one strongly dominant peptide epitope. The encephalitogenic T cells preferentially use one particular set of T‐cell receptor genes. Although MBP is a strong encephalitogen in many species, a number of other brain protein are now known to induce EAE. These include mainly myelin components (PLP, MAG, and MOG), but also, the astroglial S‐100β protein. Encephalitogenic T cells produce only inflammatory changes in the central nervous system, without extensive primary demyelination. Destruction of myelin and oligodendrocytes in these models requires additional effector mechanisms such as auto‐antibodies binding to myelin surface antigens such as the myelin‐oligodendrocyte glycoprotein.