CUTTING EDGE - B-CELL-DEFICIENT MICE DEVELOP EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS WITH DEMYELINATION AFTER MYELIN OLIGODENDROCYTE GLYCOPROTEIN SENSITIZATION

Myelin oligodendrocyte glycoprotein (MOG) induced experimental allergi c encephalomyelitis (EAE) is an animal model for the central nervous s ystem disease multiple sclerosis (MS). The roles of individual compone nts of the immune system have not been completely defined in the mouse model, and to determine the role of B cells and Abs in the induction of EAE and demyelination, B cell-deficient mu MT (H-2(b)) mice were im munized with MOG peptide 35-55, The mu MT mice were susceptible to MOG -induced EAE and developed a chronic sustained disease, with inflammat ory lesions and primary demyelination in the spinal cord, brain, and o ptic nerves, similar to that seen in wild-type C57BL/6 mice, The infla mmatory cells in the central nervous system of mu MT mice included bot h activated and memory T cells and macrophages. The data suggest that B cells and Abs are not necessary for primary demyelination in MOG-ind uced EAE in mice.