Our studies have revealed no essential differences between EAE in monkeys and MS and other CNS diseases in humans. High concentrations of BP occur early, especially if no anti-BP antibodies are also present. Lower concentrations of BP follow and may be associated with the presence of anti-BP antibodies. In EAE these antibodies come from the relatively strong peripheral sensitization to BP and enter the CSF through a damaged blood-brain barrier; in MS they come from the relatively weak immunologic stimulation probably evoked by previous attacks of the disease. Proteolytic enzymes also enter the CSF and produce peptide fragments of BP whose differing antigenic compositions permit antibodies to some fragments to coexist with other fragments unrelated antigenically but detected as "BP" in vitro. Since oligoclonal immunoglobulins (IgG) occur more often in MS than in other diseases, one can expect to find BP, anti-BP antibodies and oligoclonal IgG more often in MS, but even the combination is not specific for MS. Consideration of the temporal and immunochemical relationships as well as of the differential diagnosis provides a basis for the understanding of the significance of BP, its antibodies and other immunoglobulins in the CSF.