Multiple sclerosis is a common neurological disorder that represents a 
significant source of disability. B cells have recently emerged as a novel 
therapeutic target for multiple sclerosis. The natural development of B cells is 
characterized by an antigen-independent phase that occurs in the bone marrow and 
an antigen-dependent phase that takes place in the peripheral lymphoid tissue. 
The stage of B-cell development can be identified by the presence of specific 
cell surface markers. Checkpoints are in place to prevent self-reactive B cells 
from further development and activation. Some self-reactive B cells are able to 
escape these checkpoints, resulting in a loss of tolerance. B cells may 
contribute to systemic autoimmunity and the development of autoimmune disease 
via cytokine production, antigen presentation, and complement activation. In 
addition, B cells may trigger autoimmune disease via molecular mimicry, which 
occurs when a single B-cell receptor recognizes both a non-self antigen molecule 
and a self-molecule. Accumulating data suggest that ectopic proliferation of B 
cells in the central nervous system may also play a role. Further research is 
needed to elucidate the pathology of B cells and their role in central nervous 
system autoimmune diseases, including multiple sclerosis.