Eur J Immunol 2002 Jul;32(7):1905-13
Lyons JA, Ramsbottom MJ, Cross AH.
Department of Neurology and Neurosurgery, Washington University School of Medicine, Saint Louis, USA.
The role of B cells and antibody in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) remains controversial.
We previously demonstrated that B cells are required for EAE to be induced by the 120-amino acid extracellular domain of myelin oligodendrocyte glycoprotein (MOG).
In the present study, the role of B cells in MOG-induced EAE was further characterized.
Passive transfer of activated B cells or serum from MOG-primed wild-type (WT) mice was found to reconstitute the ability for clinical and histological EAE to be induced in MOG-immunized B cell-deficient mice.
MOG-induced EAE did not occur with transfer of B cells that had been nonspecifically activated by lipopolysaccharide or isolated from naive or myelin basic protein (MBP)-primed WT mice.
Likewise, MOG-primed serum, but not naive serum or serum from MBP-, Hen egg lysozyme-, or MOG(35-55)-primed mice, led to EAE in B cell(-/-) animals.
While both MOG-primed B cells and serum reconstituted the ability for disease induction, MOG-primed serum was much more efficient, leading to clinical and histological EAE similar to that seen in the WT.
Injection of MOG serum into healthy B cell(-/) mice 30 days after MOG immunization led to rapid appearance of clinical signs and CNS inflammation, indicating that an antigen-specific factor is necessary for initiation of CNS inflammation,and not just demyelination.
These data strongly suggest that MOG-specific antibody is critical to the initiation of MOG-induced murine EAE.