Experimental autoimmune encephalomyelitis (EAE) is an animal model for the
human autoimmune central nervous system (CNS) disease multiple sclerosis (M
S). To examine the role of B cells in EAE with a relapsing and remitting di
sease course (R-EAE) we generated (B10.PLxSJL/J)F1 mice deficient in B cell
s by disrupting their heavy chain transmembrane region (B10.PLxSJL/J)F1 mu
MT-/-. By immunizing (B10.PLxSJL/J)F1 and (B10.PLxSJL/J)F1 mu MT-/- mice wi
th the encephalitogenic N-terminal peptide Acl-11 of myelin basic protein (
MBP), we observed that B-cell deficient mice exhibited a relapsing and remi
tting disease course. Since a similar day of onset and day of first relapse
were observed these data suggest that B cells do not play a vital role in
the activation of T cells leading to the initiation of EAE, nor in the reac
tivation of T cells resulting in R-EAE. (C) 2000 Academic Press.