Chapter 3 – Role of B Cells in the Pathogenesis of Multiple Sclerosis: Mechanisms of Action

Research on the pathogenesis of multiple sclerosis (MS) has almost exclusively been conducted on T cells, more specifically CD4+ T cells. This has been based on the theory that the most effective genetic factor in MS disease is located within the major histocompatibility complex class II region. This region plays a vital and central role in the development and maturation of cell tolerance. The other reason was accessibility of experimental autoimmune encephalomyelitis, an animal model for MS. This murine model can readily be produced by injecting encephalitogenic myelin-specific T cells. The general consensus was that B cells participate in autoimmune disease pathogenesis only through production of autoantibodies. However, we now know that the role of B cells goes beyond an antibody-producing factory; they are the major antigen-presenting cells (APCs), and they produce both pro-inflammatory and anti-inflammatory cytokines in the vicinity of the affected region. Therefore, when an autoantigen-specific B cell is present, it will be the first APC to take the self-protein, break it down, and present it to T cells, priming them to become activated cells, in effect jump-starting the autoreactive chain.