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.
Pender
Michael P
MP
Neuroimmunology Research Centre, School of Medicine, The University of Queensland, Australia. m.hawes@uq.edu.au
D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000276:immunology*; D020278:Demyelinating Autoimmune Diseases, CNS / Q000276:immunology / Q000628:therapy*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000628:therapy; D053222:Fas Ligand Protein / Q000502:physiology; D005938:Glucocorticoids / Q000502:physiology; D004854:Herpesvirus 4, Human / Q000502:physiology; D006801:Humans; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000502:physiology*; D009103:Multiple Sclerosis / Q000628:therapy / Q000821:virology; D019014:fas Receptor / Q000502:physiology
D053222:Fas Ligand Protein; D005938:Glucocorticoids; D019014:fas Receptor