Treating autoimmune demyelination by augmenting lymphocyte apoptosis in the central nervous system

The elimination of autoreactive T cells from the central nervous system (CNS) by apoptosis plays an important role in switching off autoimmune attack. B-cell apoptosis in the CNS probably also has a key role in downregulating autoimmunity. Augmenting lymphocyte apoptosis in the CNS is a potential strategy for treating autoimmune CNS diseases such as multiple sclerosis. These strategies involve modulation of the physiological pro-apoptotic and anti-apoptotic pathways that control lymphocyte fate in the CNS. In the case of T cells, apoptosis can be augmented by enhancing activation-induced T-cell apoptosis through the CD95 (Fas) pathway and by inhibiting costimulation-induced anti-apoptotic pathways mediated through BCL-2 and BCL-X L.