Dept. of Neurology and Neurological Sciences, Beckman
Center for Molecular Medicine, B002, Stanford University, Stanford, California 94305, USA
steinman@stanford.edu
Multiple sclerosis results from the failure of several different regulatory
mechanisms designed to protect against autoimmunity, suggesting multiple targets
for therapeutic intervention. Three papers in this issue suggest that if tolerance
to components of the nervous system is not maintained in the thymus and autoimmunity
ensues, the extent of brain damage can be checked by blockade of glutamate
receptors on neurons and oligodendrocytes (56−70).
