The pathogenic events in multiple sclerosis (MS) that result in immune cell 
infiltration, multifocal demyelination and axonal loss have been focused by the 
strong impact of the classical MS model experimental autoimmune 
encephalomyelitis (EAE) towards the hypothesis that MS is an entirely T 
cell-mediated disease. Although conspicuous humoral immune responses have been 
known since Kabal's seminal finding of elevated immunoglobulins (Igs) in the 
cerebrospinal fluid (CSF), only in the past few years evidence derived from 
recent studies of the MS lesion of anti-myelin antibodies (Abs) in patients with 
early MS and of MS animal models has led to a renewed interest in the role for B 
cells, plasma cells and their products in the pathogenesis of MS. This review 
surveys the actual data concerning the role of the humoral immune system in MS 
and EAE and explains potential modes of action and long-time persistence in the 
inflamed brain tissue as a B cell-supportive microenvironment in MS. These 
mechanisms include the modulation of antigen presentation and costimulation to T 
cells, increased myelin opsonisation und recruitment of inflammatory cells to 
the CNS, but also immunoregulatory influences on the remyelination by 
anti-myelin B cells and Abs. So, affecting the humoral immune system in MS would 
be a reasonable therapeutic option.