Autoantibodies in demyelinating disease

I. INTRODUCTION Since the 1940s it has been known that more than 90% of multiple sclerosis (MS) patients have increased intrathecal production of immunoglobulins (Ig) in an oligoclonal pattern (1). These Igs include IgG, IgA, IgD, and IgM antibodies. In support of a role for antibodies (Abs) in the pathogenesis of MS are studies suggesting that increased concentrations of Abs in CSF of MS patients correlates with episodes of MS worsening (2) and that MS patients lacking oligoclonal bands in CSF have a more benign course (3). For many years, research into the pathogenesis of MS focused on the humoral immune system. However, in recent years, emphasis has been placed on investigating the role of the T lymphocyte in the pathological process in MS, due to the findings of activated T lymphocytes in MS plaques, T cell-subset alterations in MS blood, and the fact that an animal model for MS, experimental allergic encephalomyelitis (EAE), is initiated by myelin-reactive T cells (4).