The multiple sclerosis lesion

MS is characterized by multiple areas of myelin destruction in the central nervous system (CNS), known as plaques. CNS myelin is made by local oligodendrocytes that are gradually lost along the progression of the disease. Microscopic examination of the lesions or plaques indicates that demyelination is often accompanied by an active immune response. Inflammatory infiltrates are located perivenularlv and the cellular composition of the infiltrates varies with the age of the lesions. Acute lesions consist of macrophages, lymphocytes, plasma cells and nonmyelinated axons, while the inflammatory infiltrates arc-less pronounced in the chronic plaques. Reactive gliosis and inefficient attempts at remyelination can also be observed, suggesting that the immunological mechanisms in more chronic lesions are different from those in acute lesions.

Studies of the experimental animal model for MS, experimental autoimmune encephalomyelitis (EAE), have demonstrated that myelin basic protein (MBP)-specific, proteolipid protein (PLP)-specific or myelin oligodendroglia glycoprotein (MOG)-specific T cells mediate the autoimmune pathogenesis. The en-cephalitogenic epitopes on myelin antigens differ between species and strains and are influenced by the major histocompatibility complex (MHC) make-up of the animal. Furthermore, in some strains the en-cephalitogenic T cells use a very limited set of T cell receptor (TCR) chains in the recognition of the com plex formed by disease-associated MHC class II molecules and encephalitogenic peptides. This has led to innovative therapeutic approaches targeting each of the components specifically. In the chronic-relapsing form of EAE in the SJL/J mouse, the disease exacerbates and remits as in MS, and the murine pathology strongly resembles that seen in humans. It is possible that MS, like EAE, is caused by T lymphocytes recognizing antigens found in the CNS. However, whether the therapeutic approaches successfully used in EAE will be effective in MS is not clear, since the relationship between a specific TCR and disease is not evident. Furthermore, to date no specific antigens for the inflammatory processes in MS have been described.

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