Myelin basic protein and its antibodies in the cerebrospinal fluid in experimental allergic encephalomyelitis, multiple sclerosis and other diseases

Abstract

Myelin basic protein (BP) has been extensively studied not only as the cause of experimental allergic encephalomyelitis (EAE) but also, when released into the cerebrospinal fluid (CSF), as an indicator of activity of demyelinating diseases, especially multiple sclerosis (MS). Gutstein and Cohen¹ reported that EAE differed from MS in having antibodies to BP, but not BP itself, in the CSF. Our studies, however, 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 enzymes² also enter the CSF and produce peptide fragments of BP, whose differing antigenic compositions permit antibodies to some fragments to coexist with other fragments antigenically unrelated 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.