Abstract:

In the central nervous system (CNS), oligodendrocytes are responsible for myelination by wrapping around the axon and maintaining saltatory conduction. Damage to oligodendrocytes and the myelin sheath around nerves is termed demyelination. Multiple Sclerosis (MS) is an inflammatory demyelinating disease in the CNS characterized by immune-mediated disease, with autoimmune responses against myelin antigens and inflammation contributing to the pathogenesis of demyelination in the CNS. Although various genetic and/or non-genetic triggers such as viral infections, metabolism, or environmental factors have been associated with the pathogenesis of MS, the major cause of the disease remains unknown. To date, it is widely accepted that immune cells attack myelinated axons in the CNS, followed by demyelination and axonal degeneration. For instance, activated autoreactive T cells and myelin-specific T cells can facilitate the recruitment of macrophages by producing various cytokines and chemokines. Infiltrating inflammatory cells are activated within the CNS and interact with other immune cells and neuronal cells, resulting in oligodendroglial cell death-mediated demyelination, glial cell activation and axonal degeneration. Therefore, it has been suggested that demyelination and oligodendroglial cell death in MS is passively induced by infiltrating immune cells.