ABSTRACT
The cause of multiple sclerosis (MS) is unknown although there is a large body of experimental evidence to suggest that activated T-cells, reactive to self-antigens such as myelin basic protein, myelin oligodendrocyte glycoprotein, myelin associated glycoprotein, or proteolipid protein proliferate, and under the influence of cellular adhesion molecules and pro-inflammatory cytokines, cross the blood-brain barrier and enter the central nervous system (CNS) to produce the inflammatory lesions seen in MS patients (1,2). Other mononuclear cells such as macrophages and, to a lesser extent, B-cells are also present in active MS lesions. Together with resident CNS cells such as astrocytes and microglia, these mononuclear cells produce inflammation within the CNS and, thereby, inflict damage to both the myelin and the oligodendrocytes. Such damage may also result in irreversible axonal injury or transaction (3,4) and lead, thereby, to permanent neurological disability.
