Abstract
Quantitative and qualitative (oligoclonal band) immunoglobulin abnormalities are one of the hallmarks of multiple sclerosis. The usual explanations offered for these abnormalities include persistent antigenic stimulation, "nonsense" antibody, immunodysregulation, and nonspecific polyclonal stimulation. We propose that an intrinsic B-cell abnormality leads to the immunoglobulin disturbances--perhaps in association with one of the aforementioned mechanisms. Genetic translocations and abnormalities in the normal B cell developmental immunoglobulin rearrangements could produce a selective advantage for certain B cells or enhance transcription causing clonal proliferation with the subsequent production of oligoclonal immunoglobulin bands. Cytogenetic and molecular hybridization studies of the B cell may help answer these issues.
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