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The single most consistent laboratory abnormality found in patients with MS is increased intrathecal production of oligoclonal immunoglobulin (Ig), present in >90% of persons with definite MS.1 The increased Ig in MS CSF, described by Kabat in 1942,2 prompted a search to identify its antigenic target. However, the search for a target proved frustrating, with no infectious or autoimmune antigen being consistently identified. This frustration, together with the failure of B cells or antibody alone to induce CNS pathology in animals, led to diminished interest in B cells in MS. In the 1980s, when T lymphocytes were identified in MS plaques, T cell subset alterations were observed in MS blood, and T cells were shown to transfer the experimental allergic encephalomyelitis (EAE) animal model for MS, the role of T cells became the focus of investigation. Yet today, 150 years after the first clinico-pathologic descriptions of MS, its etiology and pathogenesis remain unknown.
The pendulum is swinging back. New data are implicating B cells and Ig in MS. In this issue, Smith-Jensen and colleagues present evidence that the …
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