In 2008, University of California, San Francisco (UCSF) researchers discovered that B cells orchestrate the inflammation of myelin that causes multiple sclerosis, leading to a new B-cell targeting therapy.

As of 2011, the strongest direct evidence for a central role of B cells in MS autoimmunity was the demonstration that peripheral B cell depletion leads to a rapid decline of disease-activity in MS. While lending formidable impact to peripheral blood B cells as mediators of disease activity, the effects of anti-CD20 treatment also seemingly challenged the paradigm of a role of antibodies in targeted central nervous system (CNS) myelin destruction.

Taken together, B cells are multi-potent players in CNS inflammation and demyelination. Our knowledge of B cell mechanisms involved in MS has grown tremendously, particularly over the past decade. This knowledge is likely to increase as more sophisticated technologies become available to solve the B cell puzzle piece-by-piece.