Abstract
Multiple Sclerosis (MS) is considered a T cell-mediated autoimmune disease of central nervous system myelin. Based on elegant experiments in an animal model of MS, experimental allergic encephalomyelitis (EAE), a number of myelin proteins and peptides derived from these can induce inflammatory demyelinating lesions. Recent studies with transgenic mice expressing human HLA-DR molecules and a myelin basic protein (MBP)-specific T cell receptor as well as data from a phase II clinical trial with an altered peptide ligand based on MBP peptide (83-99) provide convincing evidence that the pathogenetic concepts which largely stem from the above EAE studies are valid in MS, too.
Original language | English (US) |
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Pages (from-to) | 361-373 |
Number of pages | 13 |
Journal | Journal of Neural Transmission, Supplement |
Issue number | 60 |
State | Published - 2000 |
Externally published | Yes |
ASJC Scopus subject areas
- Neuroscience(all)